presentation in kidney

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• End-stage renal disease

End-stage renal disease, also called end-stage kidney disease or kidney failure, occurs when chronic kidney disease — the gradual loss of kidney function — reaches an advanced state. In end-stage renal disease, your kidneys no longer work as they should to meet your body's needs.

Your kidneys filter wastes and excess fluids from your blood, which are then excreted in your urine. When your kidneys lose their filtering abilities, dangerous levels of fluid, electrolytes and wastes can build up in your body.

With end-stage renal disease, you need dialysis or a kidney transplant to stay alive. But you can also choose to opt for conservative care to manage your symptoms — aiming for the best quality of life during your remaining time.

How kidneys work

One of the important jobs of the kidneys is to clean the blood. As blood moves through the body, it picks up extra fluid, chemicals and waste. The kidneys separate this material from the blood. It's carried out of the body in urine. If the kidneys are unable to do this and the condition is untreated, serious health problems result, with eventual loss of life.

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Early in chronic kidney disease, you might have no signs or symptoms. As chronic kidney disease progresses to end-stage renal disease, signs and symptoms might include:

• Loss of appetite
• Fatigue and weakness
• Changes in how much you urinate
• Chest pain, if fluid builds up around the lining of the heart
• Shortness of breath, if fluid builds up in the lungs
• Swelling of feet and ankles
• High blood pressure (hypertension) that's difficult to control
• Difficulty sleeping
• Decreased mental sharpness
• Muscle twitches and cramps
• Persistent itching
• Metallic taste

Signs and symptoms of kidney disease are often nonspecific, meaning they can also be caused by other illnesses. Because your kidneys can make up for lost function, signs and symptoms might not appear until irreversible damage has occurred.

When to seek care

Make an appointment with your health care provider if you have signs or symptoms of kidney disease.

If you have a medical condition that increases your risk of kidney disease, your care provider is likely to monitor your kidney function with urine and blood tests and your blood pressure during regular office visits. Ask your provider whether these tests are necessary for you.

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Healthy kidney vs. diseased kidney

A typical kidney has about 1 million filtering units. Each unit, called a glomerulus, joins a tubule. The tubule collects urine. Conditions such as high blood pressure and diabetes harm kidney function by damaging these filtering units and tubules. The damage causes scarring.

Polycystic kidney

A healthy kidney (left) removes waste from the blood and maintains the body's chemical balance. With polycystic kidney disease (right), fluid-filled sacs called cysts develop in the kidneys. The kidneys grow larger and slowly lose their ability to work as they should.

Kidney disease occurs when a disease or condition impairs kidney function, causing kidney damage to worsen over several months or years. For some people, kidney damage can continue to progress even after the underlying condition is resolved.

Diseases and conditions that can lead to kidney disease include:

• Type 1 or type 2 diabetes
• High blood pressure
• Glomerulonephritis (gloe-mer-u-low-nuh-FRY-tis) — an inflammation of the kidney's filtering units (glomeruli)
• Interstitial nephritis (in-tur-STISH-ul nuh-FRY-tis), an inflammation of the kidney's tubules and surrounding structures
• Polycystic kidney disease or other inherited kidney diseases
• Prolonged obstruction of the urinary tract, from conditions such as enlarged prostate, kidney stones and some cancers
• Vesicoureteral (ves-ih-koe-yoo-REE-tur-ul) reflux, a condition that causes urine to back up into your kidneys
• Recurrent kidney infection, also called pyelonephritis (pie-uh-low-nuh-FRY-tis)

Risk factors

Certain factors increase the risk that chronic kidney disease will progress more quickly to end-stage renal disease, including:

• Diabetes with poor blood sugar control
• Kidney disease that affects the glomeruli, the structures in the kidneys that filter wastes from the blood
• Polycystic kidney disease
• Tobacco use
• Black, Hispanic, Asian, Pacific Islander or American Indian heritage
• Family history of kidney failure
• Frequent use of medications that could be damaging to the kidney

Complications

Kidney damage, once it occurs, can't be reversed. Potential complications can affect almost any part of your body and can include:

• Fluid retention, which could lead to swelling in your arms and legs, high blood pressure, or fluid in your lungs (pulmonary edema)
• A sudden rise in potassium levels in your blood (hyperkalemia), which could impair your heart's ability to function and may be life-threatening
• Heart disease
• Weak bones and an increased risk of bone fractures
• Decreased sex drive, erectile dysfunction or reduced fertility
• Damage to your central nervous system, which can cause difficulty concentrating, personality changes or seizures
• Decreased immune response, which makes you more vulnerable to infection
• Pericarditis, an inflammation of the saclike membrane that envelops your heart (pericardium)
• Pregnancy complications that carry risks for the mother and the developing fetus
• Malnutrition
• Irreversible damage to your kidneys (end-stage kidney disease), eventually requiring either dialysis or a kidney transplant for survival

If you have kidney disease, you may be able to slow its progress by making healthy lifestyle choices:

• Achieve and maintain a healthy weight
• Be active most days
• Limit protein and eat a balanced diet of nutritious, low-sodium foods
• Control your blood pressure
• Take your medications as prescribed
• Have your cholesterol levels checked every year
• Control your blood sugar level
• Don't smoke or use tobacco products
• Get regular checkups

End-stage renal disease care at Mayo Clinic

• Goldman L, et al., eds. Chronic kidney disease. In: Goldman-Cecil Medicine. 26th ed. Elsevier; 2020. http://www.clinicalkey.com. Accessed April 27, 2021.
• Chronic kidney disease (CKD). National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd#:~:text=Chronic%20kidney%20disease%20(CKD)%20means,family%20history%20of%20kidney%20failure. Accessed April 26, 2021.
• Rosenberg M. Overview of the management of chronic kidney disease in adults. https://www.uptodate.com/contents/search. Accessed April 26, 2021.
• Chronic kidney disease. Merck Manual Professional Version. https://www.merckmanuals.com/professional/genitourinary-disorders/chronic-kidney-disease/chronic-kidney-disease?query=Chronic%20kidney%20disease. Accessed April 26, 2021.
• Office of Patient Education. Chronic kidney disease treatment options. Mayo Clinic; 2020.
• Are you at increased risk for chronic kidney disease (CKD)? National Kidney Foundation. https://www.kidney.org/atoz/content/atriskckd. Accessed May 25, 2021.
• Warner KJ. Allscripts EPSi. Mayo Clinic. April 12, 2021.
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Author: Jana Vasković, MD • Reviewer: Dimitrios Mytilinaios, MD, PhD Last reviewed: November 03, 2023 Reading time: 23 minutes

The kidneys are bilateral organs placed retroperitoneally in the upper left and right abdominal quadrants and are part of the urinary system . Their shape resembles a bean, where we can describe the superior and inferior poles, as well as the major convexity pointed laterally, and the minor concavity pointed medially.

The main function of the kidney is to eliminate excess bodily fluid, salts and byproducts of metabolism – this makes kidneys key in the regulation of acid-base balance, blood pressure, and many other homeostatic parameters.

This article will discuss the anatomy and major functions of the kidney.

External anatomy

Posterior surface relations, internal anatomy, veins and lymphatics, innervation, third kidney, renal agenesis, kidney stones, acute kidney failure.

The kidney is a very important organ in regards to body homeostasis . It participates in vital processes such as regulation of blood osmolarity and pH, regulation of blood volume and blood pressure, production of hormones, and filtration of foreign substances.

In general, the amount of blood in the body is 5 liters. Any excessive amount of fluid will increase the pressure on the arterial wall and cause the blood pressure to rise ( hypertension ). Luckily, the kidneys also feel this increase of pressure, and in cases when this happens, they increase the filtration rate of blood and production of urine, which subsequently leads to the increase fluid excretion and decrease of blood pressure. Of course, if the situation is the other way around (less than 5 liters of blood), blood pressure is too low (hypotension). Hypotension is a stimulus for the kidneys to increase the retention of fluid and thus increase blood pressure.

Besides blood volume and pressure regulation, kidneys also participate in the production of calcitriol (the active form of vitamin D). Also, in situations with notable blood losses, kidneys release a hormone called erythropoietin , which stimulates bone marrow to produce more blood cells.

Cells in our body constantly produce hydrogen ions. An increased amount of hydrogen ions can acidify the blood and cause a state called acidosis . Kidneys have a special system for the excretion of hydrogen ions, and in that way consistently maintain the pH of blood at 7.4. The opposite situation is possible too, if the kidneys excrete too many hydrogen ions, the pH of blood becomes too alkaline, and leads to a state called alkalosis .

This is just a peek into the kidney physiology . In order to understand the functions of the kidney, we must first learn its anatomy.

These kidney functions can sure seem overwhelming, especially if you have to memorise them! But here is a neat little mnemonic to help. Just remember ' A WET BED ', which stands for:

• Maintaining A CID-base balance
• Maintaining W ATER balance
• E LECTROLYTE balance
• T OXIN removal
• B LOOD Pressure control
• Making E RYTHROPOIETIN
• Vitamin D metabolism

The kidneys have their anterior and posterior surfaces. The anterior surface faces towards the anterior abdominal wall , whereas the posterior surface is facing the posterior abdominal wall. These surfaces are separated by the edges of the kidney, which are the major convexity laterally, and minor concavity medially. The center of the minor concavity is marked as the hilum of the kidney where the renal artery enters the kidney, and the renal vein and ureter leave the kidney. Learning a quick  mnemonic  ' VAD ' can help you remember these structures (renal V ein, renal A rtery, D uct a.k.a ureter).

The kidneys are positioned retroperitoneally, meaning that they are not wrapped with the peritoneal layers the way most abdominal organs are, but rather are placed behind it. On the other hand, kidneys do have relations with peritoneum , or precisely with the specific organs that are covered with peritoneum which are placed directly adjacent to the kidneys.

Learn more about the anatomy of the kidneys and the urinary system with our urinary system quizzes and labeled diagrams.

To quiz yourself on the anatomy of the kidneys take our quiz or, take a look at the study unit below:

If we wanted to examine someone’s kidneys with ultrasound, we definitely must know where to find them. Since they are located deep retroperitoneally , the easiest way to examine them is from the patient’s back. 

The kidneys are located between the transverse processes of T12-L3 vertebrae, with the left kidney typically positioned slightly more superiorly than the right. This is because the liver and the stomach offset the symmetry of the abdomen , with the liver forcing the right kidney a bit down, and the stomach forcing the left kidney a bit up. The superior poles (extremities) (T12) of both kidneys are more medially pointed towards the spine than the inferior poles (extremities) (L3). The hilum of the kidney usually projects at the level of the L2 vertebra. Thus, the ureter is seen paravertebrally starting from the L2 and going downwards.

Now let’s pay attention to the borders of the kidneys. A bean-like structure like the kidney has two borders: medial and lateral. The lateral border is directed towards the periphery, while the medial border is the one directed towards the midline. The medial border of the kidney contains a very important landmark called the hilum of the kidney, which is the entry and exit point for the kidney vessels and ureter.

The most superior vessel is the renal vein which exits the kidney, just under it is the renal artery that enters in, and under the artery is the exiting ureter . Alternatively, the anterior to posterior orientation follows the same pattern: renal vein, renal artery and ureter. It is important to remember this order of vessels and ducts since this is the only thing that will make you able to orient the kidney and differentiate the left one from the right when they are outside of the cadaver. 

The kidney tissue is protected by three layers that entirely surround the kidney: 

• The fibrous capsule ( renal capsule )
• The perirenal fat body (a.k.a. perinephric fat)
• The renal fascia which besides the kidneys also encloses the suprarenal gland and its surrounding fat. 

Outside the fascia is the most superficial layer – a layer of fat tissue called the pararenal (/paranephric) fat body. This layer sits posteriorly and posterolaterally to each kidney and separates it from the muscles of the abdominal wall. 

Now that we’ve mastered the borders, it will be easier to take a closer look at the anatomical relations that the kidneys share with other abdominal structures.

Right kidney anterior surface

After looking at the overview of the kidneys in situ, it may seem as they are cluttered with all abdominal organs. Yet, the relations of the kidneys with other organs are often found in Anatomy tests. For that reason, we got you covered with this topic nicely and concisely. Let’s start with the right kidney anterior surface.

• The highest portion of the superior pole is covered with the right suprarenal gland
• The superior one-half of the anterior surface is in contact with the layer of peritoneum that separates it from the liver. This potential space that separates the liver from the right kidney is called the hepatorenal pouch of Morison . Under normal conditions, this pouch is empty, but certain pathological conditions, such as ascites or hemoperitoneum, can cause fluid to collect within the pouch. This can be visualized with ultrasound or CT.
• At exactly the center of the anterior surface, imagine a horizontal stripe that extends from the medial concavity toward the center of the lateral convexity – that is the area of the kidney that is directly touched by the retroperitoneal posterior wall of the descending duodenum
• The lateral part of the inferior pole is directly contacted with the right colic flexure (also known as the hepatic flexure) which is also retroperitoneal at this part
• The rest of the inferior pole is associated with the peritoneum of the small intestine , more precisely the jejunum

Left kidney anterior surface

Since the abdominal organs are not paired, the left kidney is not related to the same organs as the right kidney.

The anterior surface of the left kidney, has the following anatomical relations:

• Just like the right kidney, the highest part of the superior pole of the left is also covered with the left suprarenal gland F
• The inferior portion of the superior pole contacts with the peritoneum of the stomach (medially) and spleen (laterally)
• Just inferior to the stomach and spleen impression, is where the left kidney directly contacts the pancreas
• The lateral part of the inferior half of the anterior surface is directly associated with the left colic flexure (also known as the splenic flexure) and descending colon
• The medial part of the inferior half and the inferior pole are contacted by the peritoneum of the jejunum

The posterior surfaces of both kidneys are related to certain neurovascular structures and muscles:

• 1 Artery: subcostal artery
• 2 Bones: 11th and 12th ribs
• 3 Nerves: subcostal, iliohypogastric , and ilioinguinal nerves
• 4 Muscles: diaphragm , psoas major , quadratus lumborum , transversus abdominis

You can easily remember these with the mnemonic: “1-2-3-4 All Boys Need Muscle”.

The superior half of each kidney is covered by the diaphragm , which is why the kidneys move up and down during respiration

The muscular relations of the inferior half are easy to remember by dividing the kidney surface into three vertical stripes, where the medial stripe represents the impression of the psoas major muscle, the central stripe the quadratus lumborum, and the lateral stripe the transversus abdominis muscle.

The parenchyma of the kidney consists of the outer renal cortex , and inner renal medulla.

The main unit of the medulla is the renal pyramid . There are 8-18 renal pyramids in each kidney, that on the coronal section look like triangles lined next to each other with their bases directed toward the cortex and apex to the hilum. The apex of the pyramid projects medially toward the renal sinus. This apical projection is called the renal papilla and it opens to a  minor calix . Several minor calices unite to form a major calix . Usually, there are two to three major calices in the kidney (superior, middle, and inferior), which again unite to form the renal pelvis from which the ureter emerges and leaves the kidney through the hilum. The pyramids are separated by extensions of the cortex called the renal columns .

The pyramids contain the functional units of the kidney, the nephrons , which filter blood in order to produce urine which then is transported through a system of the structures called calices which then transport the urine to the ureter. So the pyramids represent the functional tissue that creates urine, whereas the calices are the beginning of the ureter and transport the urine to it.

Each time a professor says 'nephron', a student gets a headache. For most of the students, the nephron is a mystical complexed structure that may be hard to understand. It doesn't have to be that way. Let's see what is nephron and how it is structured, so you can remember it for good.

Ultrastructurally, the nephron is the functional representative of the kidney. Each nephron contains a renal corpuscle , which is the initial component that filters the blood, and a renal tubule that processes and carries the filtered fluid to the system of calices. The renal corpuscle has two components: the glomerular (Bowman’s) capsule in which sits the glomerulus.

The glomerulus is actually a web of arterioles and capillaries, with a special filter which filters the blood that runs through the capillaries, the glomerular membrane. The vessel which brings blood into the glomerulus is the afferent arteriole , whereas the vessel that carries the rest of the blood out that hasn’t been filtered out of the glomerulus is called the efferent arteriole . 

The glomerular membrane is designed in a way in which it is not permeable for big and important molecules in blood, such as plasma proteins, but it is permeable to the smaller substances such as sodium, potassium, amino acids and many others. It is also permeable for the products of the metabolism, such are creatinine and drug metabolites.

So in the filtered fluid that goes to the renal tubule, we have both necessary and unnecessary substances. Because of this, the tubules are designed in a way that they reabsorb the necessary substances, (sodium, potassium, and amino acids as mentioned before) and carries them back to the blood; whereas they do not absorb but rather secrete unnecessary substances such as creatinine and drug metabolites for excretion from the body.

In this way, the consistency of blood is preserved and no important substances are lost. On the other hand, the products of cellular metabolism and drug metabolites are eliminated from the blood which prevents their depositing in the body and potential toxicity. This is why the kidney is essential for the circulatory hemostasis.

Learn more about the nephron in the following study unit or take our custom quiz to see what you know already:

Vasculature and lymphatic drainage

Each kidney is supplied by a single renal artery , which is a direct lateral branch of the abdominal aorta. Both renal arteries, left and right, arise just below the superior mesenteric artery, with the left renal artery positioned slightly superiorly to the right one. The left artery has a short way to the left kidney, whereas the right has to go behind the inferior vena cava in order to reach the right kidney. In addition to the renal artery, accessory renal arteries are present too. They are branches of the abdominal aorta and all together are called the extrahilar renal arteries.

When the renal arteries enter the kidney through the hilum, they split into anterior and posterior branches. The posterior branch supplies the posterior part of the kidney, whereas the anterior branch arborizes into five segmental arteries, each supplying a different renal segment. The segmental arteries then branch into the interlobar arteries , which further branch into the arcuate arteries . Finally, the arcuate arteries branch into the interlobular arteries which branch off even further by giving afferent arterioles to run blood past the glomerulus for blood filtration. It is notable that the kidney has a very rich blood supply .

You can test yourself on the renal arteries with our quiz.

Each kidney has a single renal vein which conducts the blood out of the kidney and is positioned anterior to the artery. The renal veins empty to the inferior vena cava, so the right vein is shorter because the inferior vena cava runs closer to the right kidney. The left renal vein passes anteriorly to the aorta just below the trunk of the superior mesenteric artery , which is risky because it can be compressed by one of those two. This is called the nutcracker phenomenon. Concerning lymphatic drainage, each kidney drains into the lateral aortic (lumbar) lymph nodes , which are placed around the origin of the renal artery.

Note that the left renal vein receives blood from the left suprarenal and left testicular veins . The left testicular vein must ascend higher and it drains to the left renal vein at a right angle, unlike the right testicular vein which joins the inferior vena cava directly. This can cause varicocele of the left testicle because gravity works against the column of the blood in the left testicular vein.

Furthermore, since the left renal vein passes between the superior mesenteric artery and the abdominal aorta, an enlargement of the superior mesenteric artery can compress the left renal vein and cause an obstruction of drainage from all three structures that use the left renal vein for drainage (left suprarenal gland, left kidney, and left testicle). This significantly affects the testicle, since an obstruction of drainage causes an obstruction of fresh arterial blood inflow, which can result in the infarction of testicular tissue. This specific condition is called the nutcracker phenomenon .

The kidneys are innervated by the renal plexus. This plexus provides input from:

• the sympathetic nervous system from the lower thoracic splanchnic nerves for the regulation of the vascular tone, and from 
• the parasympathetic nervous system as well, through the vagus nerve .

The sensory nerves from the kidney travel to the spinal cord at the levels T10-T11, which is why the pain in the flank region always rises suspicions that something is wrong with the corresponding kidney.

Clinical relations

There are many clinical states related to kidney malfunction. Some of them are congenital, such as a third kidney , which is usually atrophic. In other cases, both kidneys can be fused, usually at the inferior poles, which is a congenital state called the horseshoe kidney . There is no specific treatment for fused kidneys and the only option is to treat the pathologies that affect them during life.

Sometimes, one or both kidneys fail to develop, which causes unilateral or bilateral renal agenesis . People with unilateral agenesis often are unaware that they lack one kidney until an accidental discovery, since the one kidney that they have is able to functionally compensate for the other. On the other hand, babies with bilateral agenesis cannot survive without an immediate kidney transplant.

Other common kidney conditions are acquired through life, and one of the most common is nephrolithiasis (kidney stones). This refers to the forming of the stones within the system of calices because of too much calcium or uric acid into the filtrate. The calcium or uric acid will precipitate and form stones. The stones can move into the ureter and literally get stuck there because the lumen of the ureter is much smaller compared to the calices, which is very painful for the patient. Kidney stones are most often treated by ultrasound shock therapy, during which high-frequency radio waves break the stone into smaller pieces that can be passed naturally into the urine. Other methods include classical surgical removal of the stone, either through the ureter or by open surgery.

Other malfunctions of the kidney are presented through acute kidney failure , a serious and urgent medical condition. It can be caused by a variety of factors, but most often arises because of the ischemia of the kidney and the toxic effect of some medications, resulting in the failure of all kidney functions. We’ve mentioned that the most important functions of the kidney are the regulation of the blood homeostasis and blood pressure, so acute kidney failure can lead to a quick fall of blood pressure which presents as a state of shock.

References:

• R. L. Drake, A. W. Vogl, A. W. M. Mitchell: Gray’s Anatomy for Students, 3rd edition, Churchill-Livingstone (2018), p. 373-380
• K. L. Moore, A. F. Dalley II, A. M. R. Agur: Clinically Oriented Anatomy, 7th edition, Lippincott Williams & Wilkins (2014), p. 292

Illustrations:

• Kidney structure (overview) - Mohammed Albakkar
• Kidneys in situ (overview) - Johannes Reiss
• Internal anatomy of the kidney (overview) - Mohammed Albakkar
• Nephron (overview) - Mohammed Albakkar
• Arteries of the kidney (overview) - Abdulmalek Albakkar
• Kidneys in a cadaver - Prof. Carlos Suárez-Quian

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The Kidneys

Written by Oliver Jones

Last updated April 16, 2024 • 62 Revisions •

The kidneys  are bilateral bean-shaped organs, reddish-brown in colour and located in the posterior abdomen. Their main function is to filter and excrete waste products from the blood. They are also responsible for water and electrolyte balance in the body.

Metabolic waste and excess electrolytes are excreted by the kidneys to form  urine . Urine is transported from the kidneys to the bladder by the ureters . It leaves the body via the urethra , which opens out into the perineum  in the female and passes through the penis in the male.

In this article we shall look at the anatomy of the kidneys – their anatomical position, internal structure and vasculature.

Fig 1 Overview of the urinary tract.

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Anatomical position.

The kidneys lie retroperitoneally (behind the peritoneum) in the abdomen, either side of the vertebral column.

They typically extend from  T12 to L3 , although the right kidney is often situated slightly lower due to the presence of the liver. Each kidney is approximately three vertebrae in length.

The  adrenal glands sit immediately superior to the kidneys within a separate envelope of the renal fascia .

Dissection Images

Kidney Structure

The kidneys are encased in complex layers of fascia and fat. They are arranged as follows (deep to superficial):

• Renal capsule – tough fibrous capsule.
• Perirenal fat – collection of extraperitoneal fat.
• Renal fascia (also known as Gerota’s fascia or perirenal fascia) – encloses the kidneys and the suprarenal glands.
• Pararenal fat – mainly located on the posterolateral aspect of the kidney.

Fig 2 The external coverings of the kidney.

Internally, the kidneys have an intricate and unique structure. The renal parenchyma can be divided into two main areas – the outer cortex and inner medulla . The cortex extends into the medulla, dividing it into triangular shapes – these are known as renal pyramids .

The apex of a renal pyramid is called a renal papilla . Each renal papilla is associated with a structure known as the minor calyx , which collects urine from the pyramids. Several minor calices merge to form a major calyx . Urine passes through the major calices into the renal pelvis , a flattened and funnel-shaped structure. From the renal pelvis, urine drains into the ureter, which transports it to the bladder for storage.

The medial margin of each kidney is marked by a deep fissure, known as the renal hilum . This acts as a gateway to the kidney – normally the renal vessels and ureter enter/exit the kidney via this structure.

Fig 3 The internal structure of the kidney.

Anatomical Relations

The kidneys sit in close proximity to many other abdominal structures which are important to be aware of clinically:

Arterial Supply

The kidneys are supplied with blood via the   renal arteries , which arise directly from the abdominal aorta, immediately distal to the origin of the  superior mesenteric artery .  Due to the anatomical position of the abdominal aorta (slightly to the left of the midline), the right renal artery is longer, and crosses the vena cava posteriorly.

The renal artery enters the kidney via the renal hilum. At the hilum level, the renal artery forms an anterior and a posterior division, which carry 75% and 25% of the blood supply to the kidney, respectively. Five segmental arteries originate from these two divisions.

The avascular plane of the kidney (line of Brodel) is an imaginary line along the lateral and slightly posterior border of the kidney, which delineates the segments of the kidney supplied by the anterior and posterior divisions. It is an important access route for both open and endoscopic surgical access of the kidney, as it minimises the risk of damage to major arterial branches.

Note: The renal artery branches are anatomical end arteries – there is no communication between vessels. This is of crucial importance; as trauma or obstruction in one arterial branch will eventually lead to ischaemia and necrosis of the renal parenchyma supplied by this vessel.

The segmental branches of the renal undergo further divisions to supply the renal parenchyma:

• Each segmental artery divides to form  interlobar arteries . They are situated either side every renal pyramid.
• These interlobar arteries undergo further division to form the  arcuate arteries .
• At 90 degrees to the arcuate arteries, the  interlobular arteries  arise.
• The interlobular arteries pass through the cortex, dividing one last time to form  afferent arteriole s .
• The afferent arterioles form a capillary network, the glomerulus, where filtration takes place. The capillaries come together to form the efferent arterioles.

In the outer two-thirds of the renal cortex, the efferent arterioles form what is a known as a  peritubular network , supplying the nephron tubules with oxygen and nutrients. The inner third of the cortex and the medulla are supplied by long, straight arteries called vasa recta.

Fig 4 Arterial and venous supply to the kidneys.

Fig 5 Arterial supply to the kidney can be divided into five segments.

Clinical Relevance

Variation in arterial supply to the kidney.

The kidneys present a great variety in arterial supply; these variations may be explained by the ascending course of the kidney in the retroperitoneal space , from the original embryological site of formation (pelvis) to the final destination (lumbar area). During this course, the kidneys are supplied by consecutive branches of the iliac vessels and the aorta.

Usually the lower branches become atrophic and vanish while new, higher ones supply the kidney during its ascent. Accessory arteries are common (in about 25% of patients). An accessory artery is any supernumerary artery that reaches the kidney. If a supernumerary artery does not enter the kidney through the hilum, it is called aberrant .

Fig 6- Supernumerary arteries of the kidney,

Venous Drainage

The kidneys are drained of venous blood by the left and right renal veins . They leave the renal hilum anteriorly to the renal arteries, and empty directly into the inferior vena cava.

As the vena cava lies slightly to the right, the left renal vein is longer, and travels anteriorly to the abdominal aorta below the origin of the superior mesenteric artery. The right renal artery lies posterior to the inferior vena cava.

Lymph from the kidney drains into the lateral aortic (or para-aortic) lymph nodes , which are located at the origin of the renal arteries.

Congenital Abnormalities of the Kidneys

Pelvic kidney.

In utero, the kidneys develop in the pelvic region and ascend to the lumbar retroperitoneal area. Occasionally, one of the kidneys can fail to ascend and remains in the pelvis – usually at the level of the common iliac artery.

Horseshoe Kidney

A  horseshoe kidney  (also known as a cake kidney or fused kidney) is where the two developing kidneys fuse into a single horseshoe-shaped structure.

This occurs if the kidneys become too close together during their ascent and rotation from the pelvis to the abdomen – they become fused at their lower poles (the isthmus ) and consequently become ‘stuck’ underneath the inferior mesenteric artery .

This type of kidney is still drained by two ureters (although the pelvices and ureters remain anteriorly due to incomplete rotation) and is usually asymptomatic, although it can be prone to  obstruction .

Renal Cell Carcinoma

The kidney is often the site of tumor development, most commonly renal cell carcinoma.

Due to the segmental vascular supply of the kidney it is often feasible to ligate the relative arteries and veins and remove the tumour with a safe zone of healthy surrounding parenchyma ( partial nephrectomy ) without removing the entire kidney or compromising its total vascular supply by ischaemia.

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Acute Kidney Injury (AKI) Clinical Presentation

• Author: Biruh T Workeneh, MD, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
• Sections Acute Kidney Injury (AKI)
• Practice Essentials
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Complications
• Approach Considerations
• Kidney Function Studies
• CBC, Peripheral Smear, and Serology
• Fractional Excretion of Sodium and Urea
• Bladder Pressure
• Emerging Biomarkers
• Furosemide Stress Testing
• Ultrasonography
• Nuclear Scanning
• Aortorenal Angiography
• Kidney Biopsy
• Vasodilators
• Dietary Modification
• Prevention of Contrast-Induced Nephropathy
• Long-Term Monitoring
• Prevention of Perioperative Nephropathy
• Medication Summary
• Diuretics, Loop
• Inotropic Agents
• Calcium Channel Blockers
• Antidotes, Other
• Questions & Answers
• Media Gallery

A detailed and accurate history is crucial for diagnosing acute kidney injury (AKI) and determining treatment. Distinguishing AKI from chronic kidney disease is important, yet making the distinction can be difficult; chronic kidney disease is itself an important risk factor for AKI. [ 64 ]  A history of chronic symptoms—months of fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus—suggests chronic kidney disease. AKI can cause identical symptoms, but over a shorter course.

It is important to elicit a history of any of the following etiologic factors:

• Volume restriction (eg, low fluid intake, gastroenteritis)
• Nephrotoxic drug ingestion (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], aminoglycosides) [ 64 ]
• Exposure to iodinated contrast agents within the past week  [ 64 ]
• Trauma or unaccustomed exertion
• Blood loss or transfusions
• Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
• Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners

People with the following comorbid conditions are at a higher risk for developing AKI:

• Hypertension
• Chronic heart failure
• Diabetes mellitus
• Liver disease
• Obesity [ 65 , 66 , 67 , 68 ]
• Multiple myeloma
• Chronic infection
• Myeloproliferative disorder
• Connective tissue disorders
• Autoimmune diseases

Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.

Because of a decrease in functioning nephrons, even a trivial nephrotoxic insult may cause AKI to be superimposed on chronic kidney insufficiency.

AKI has a long differential diagnosis. The history can help to classify the pathophysiology of AKI as prerenal, intrinsic, or postrenal failure, and it may suggest some specific etiologies. (See Overview/Etiology .)

Prerenal failure

Patients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced heart failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.

Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.

Intrinsic kidney failure

Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI. Nephritic syndrome of hematuria, edema, and hypertension indicates a glomerular etiology for AKI. Query about prior throat or skin infections. Acute tubular necrosis (ATN) should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.

A careful search for exposure to nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents). Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis (muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood transfusion). Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.

Postrenal failure

Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of urgency, frequency, and hesitancy. These patients may present with asymptomatic, high-grade urinary obstruction because of the chronicity of their symptoms. In other cases, a history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of obstruction.

Flank pain and hematuria should raise concern about renal calculi or papillary necrosis as the source of urinary obstruction. Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility that crystals of these medications have caused tubular obstruction.

Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of AKI. Clues may be found in any of the following:

Cardiovascular system

Pulmonary system.

Skin examination may reveal the following:

• Livido reticularis, digital ischemia, butterfly rash, palpable purpura - Systemic vasculitis
• Maculopapular rash - Allergic interstitial nephritis
• Track marks (ie, intravenous drug abuse) - Endocarditis

Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AK. Infectious diseases, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), and embolic phenomena can produce typical cutaneous changes.

Eyes and ears

Eye examination may reveal the following:

• Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune vasculitis
• Jaundice - Liver diseases
• Band keratopathy (ie, hypercalcemia) - Multiple myeloma
• Signs of diabetes mellitus
• Signs of hypertension
• Atheroemboli - Retinopathy

Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis. Findings suggestive of severe hypertension, atheroembolic disease, and endocarditis may be observed on careful examination of the eyes.

Ear examination may reveal the following:

• Hearing loss - Alport disease, aminoglycoside toxicity, platinum compound toxicity
• Mucosal or cartilaginous ulcerations - Granulomatosis with polyangiitis (Wegener granulomatosis)

The most important part of the physical examination is the assessment of cardiovascular and volume status. The physical examination must include the following:

• Pulse rate and blood pressure measured in the supine and the standing position
• Close inspection of the jugulovenous pulse
• Careful examination of the heart and lungs, skin turgor, and mucous membranes
• Assessment for peripheral edema

Cardiovascular examination may reveal the following:

• Irregular rhythms (ie, atrial fibrillation) - Thromboemboli
• Murmurs - Endocarditis
• Pericardial friction rub - Uremic pericarditis
• Increased jugulovenous distention, rales, S 3 - Heart failure

In hospitalized patients, accurate daily records of fluid intake and urine output, as well as daily measurements of patient weight, are important. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia. Severe heart failure may also cause hypotension. Although patients with heart failure may have low blood pressure, volume expansion is present and effective renal perfusion is poor, which can result in AKI.

Severe hypertension with kidney failure suggests one of the following disorders:

• Renovascular disease
• Glomerulonephritis
• Atheroembolic disease
• Subcapsular hematoma

Abdominal examination may reveal the following:

• Pulsatile mass or bruit - Atheroemboli
• Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis
• Pelvic, rectal masses; prostatic hypertrophy; distended bladder – Urinary obstruction
• Limb ischemia, edema - Rhabdomyolysis

Abdominal examination findings can be useful in helping to detect obstruction at the bladder outlet as the cause of AKI; such obstruction may be due to cancer or to an enlarged prostate.

The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI. The presence of an epigastric bruit suggests renal vascular hypertension, which may predispose to AKI.

Pulmonary examination may reveal the following:

• Rales - Goodpasture syndrome, granulomatosis with polyangiitis
• Hemoptysis - Granulomatosis with polyangiitis

AKI may result in the following types of complications:

• Cardiovascular
• Gastrointestinal

Cardiovascular complications

Cardiovascular complications (eg, heart failure, myocardial infarction, arrhythmias, cardiac arrest) have been observed in as many as 35% of patients with AKI. Fluid overload secondary to oliguric AKI is a particular risk for elderly patients with limited cardiac reserve. Additionally, AKI is associated with electrolyte and acid-base imbalance that can increase the risk of arrhythmias and can decrease myocardial contractility. In cardiac patients who experience AKI either in the setting of acute decompensated heart failure or cardiac surgery, AKI is associated with worse morbidity and mortality. [ 69 ]

Pericarditis is a relatively rare complication of AKI. When pericarditis complicates AKI, consider additional diagnoses, such as systemic lupus erythematosus (SLE) and hepatorenal syndrome.

AKI also can be a complication of cardiac diseases, such as endocarditis, decompensated heart failure, or atrial fibrillation with emboli. Cardiac arrest in a patient with AKI should always arouse suspicion of hyperkalemia. Many authors recommend that in addition to Acute Cardiac Life Support (ACLS) measures in patients with pulseless electrical activity (PEA), a trial of intravenous calcium chloride (or gluconate) should be considered in patients with AKI with known or suspected hyperkalemia.

Pulmonary complications

Pulmonary complications have been reported in approximately 54% of patients with AKI and are the single most significant risk factor for death in these patients. Proposed mechanisms for acute lung injury during AKI include hypervolemia, increased proinflammatory cytokine levels, leukocyte infiltration, and increased pulmonary vascular permeability. In addition, the following diseases commonly present with simultaneous pulmonary and renal involvement:

• Goodpasture syndrome
• Granulomatosis with polyangiitis (Wegener granulomatosis)
• Polyarteritis nodosa
• Cryoglobulinemia
• Sarcoidosis

Hypoxia commonly occurs during hemodialysis and can be particularly significant in patients with pulmonary disease. This dialysis-related hypoxia is thought to occur secondary to white blood cell (WBC) lung sequestration and alveolar hypoventilation.

Gastrointestinal complications

Nausea, vomiting, and anorexia are frequent complications of AKI and represent one of the cardinal signs of uremia. GI bleeding occurs in approximately one-third of patients with AKI. Most episodes are mild, but GI bleeding accounts for 3-8% of deaths in patients with AKI.

Pancreatitis

Mild hyperamylasemia is commonly seen in AKI. Elevation of baseline amylase concentrations can complicate the diagnosis of pancreatitis in patients with AKI. Lipase measurement, frequently suppressed in AKI, should be considered in this light when there is suspicion of pancreatitis. Pancreatitis has been reported as a concurrent illness with AKI in patients with atheroemboli, vasculitis, and sepsis from ascending cholangitis.

Jaundice frequently complicates AKI. Etiologies of jaundice with AKI include hepatic congestion, blood transfusions, and sepsis.

Hepatitis occurring concurrently with AKI should prompt consideration of the following disorders in the differential diagnosis:

• Common bile duct obstruction
• Fulminant hepatitis 
• Hepatitis B– and hepatitis C–associated glomerulonephritis
• Leptospirosis
• Medication toxicity (eg, acetaminophen toxicity )
• Amanita phalloides poisoning

Infectious complications

Infections commonly complicate the course of AKI and have been reported to occur in as many as 33% of patients with AKI. It is attributed to possible altered cytokine homeostasis and immune cell dysfunction associated with AKI. The most common sites of infection are the pulmonary and urinary tracts. Infections are the leading cause of morbidity and death in patients with AKI. Various studies have reported mortality rates of 11-72% in infections complicating AKI.

Neurologic complications

Neurologic symptoms of uremia have been reported in approximately 38% of patients with AKI. Neurologic sequelae include lethargy, somnolence, reversal of the sleep-wake cycle, and cognitive or memory deficits. Focal neurologic deficits are rarely caused solely by uremia.

The pathophysiology of neurologic symptoms in AKI is still unknown but is partially attributed to the possible accumulation of neurotoxic metabolites that can lead to an imbalance in cellular water transportation and disturbance of the blood-brain barrier. However, these symptoms do not correlate well with levels of BUN or creatinine.

A number of diseases can present with concurrent neurologic and renal manifestations, including the following:

• Thrombotic thrombocytopenic purpura (TTP)
• Hemolytic-uremic syndrome (HUS)
• Endocarditis
• Malignant hypertension

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• Pigmented, muddy brown, granular casts are visible in the urine sediment of a patient with acute tubular necrosis (400x magnification).
• Photomicrograph of a kidney biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Features suggesting acute tubular necrosis are the patchy or diffuse denudation of the renal tubular cells with loss of brush border (blue arrows); flattening of the renal tubular cells due to tubular dilation (orange arrows); intratubular cast formation (yellow arrows); and sloughing of cells, which is responsible for the formation of granular casts (red arrow). Finally, intratubular obstruction due to the denuded epithelium and cellular debris is evident (green arrow); note that the denuded tubular epithelial cells clump together because of rearrangement of intercellular adhesion molecules.
• Table 1. RIFLE Classification System for Acute Kidney Injury
• Table 2. Acute Kidney Injury Network Classification/Staging System for AKI 

Contributor Information and Disclosures

Biruh T Workeneh, MD, FASN Professor of Medicine, University of Texas MD Anderson Cancer Center Biruh T Workeneh, MD, FASN is a member of the following medical societies: American Society of Nephrology , National Kidney Foundation Disclosure: Nothing to disclose.

Omar Mamlouk, MBBS Instructor, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center Omar Mamlouk, MBBS is a member of the following medical societies: American Society of Nephrology , American Society of Onconephrology , National Kidney Foundation , Texas Medical Association Disclosure: Nothing to disclose.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science , American Society for Bone and Mineral Research , American Society of Nephrology , American Society of Transplantation , International Society of Nephrology , Kentucky Medical Association , National Kidney Foundation Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc.

Vecihi Batuman, MD, FASN Professor of Medicine, Section of Nephrology-Hypertension, Deming Department of Medicine, Tulane University School of Medicine Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians , American Society of Hypertension , American Society of Nephrology , Southern Society for Clinical Investigation Disclosure: Nothing to disclose.

Mahendra Agraharkar, MD, MBBS, FACP, FASN Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians , American Society of Nephrology , National Kidney Foundation Disclosure: Nothing to disclose.

Rajiv Gupta, MD Assistant Professor, Department of Medicine, Texas A&M University College of Medicine; Consulting Staff, Veterans Affairs Medical Center Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha , American College of Cardiology , Society for Cardiovascular Angiography and Interventions Disclosure: Nothing to disclose.

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Aruna Agraharkar, MD, FACP is a member of the following medical societies: American Medical Assocation

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science , American Federation for Medical Research , American Society for Biochemistry and Molecular Biology , American Society for Bone and Mineral Research , American Society of Nephrology , American Society of Transplantation , International Society of Nephrology , Kentucky Medical Association , National Kidney Foundation , and Phi Beta Kappa

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Laura Lyngby Mulloy, DO, FACP Professor of Medicine, Chief, Section of Nephrology, Hypertension, and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia

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Anatomy of The Kidney

Jul 24, 2014

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Anatomy of The Kidney. Objectives. By the end of the lecture, the student should be able to describe the: Anatomical features of the kidneys: position, extent, relations, hilum, peritoneal coverings Internal structure of the kidneys: Cortex, medulla and renal sinus

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• inguinal nerves
• renal cortex
• spinal cord
• renal columns project
• aortic lymph nodes

Presentation Transcript

Objectives By the end of the lecture, the student should be able to describe the: • Anatomical features of the kidneys: position, extent, relations, hilum, peritoneal coverings • Internal structure of the kidneys: Cortex, medulla and renal sinus • The vascular segments of the kidneys • The blood supply and lymphatics of the kidneys.

Location & Position of the kidneys • The kidneys are retroperitoneal paired organs • Each kidney lies lateral to the vertebral column, on the posterior abdominal wall largely under cover of the costal margin • In the supine position, the kidneys extend from approximately T12 vertebra superiorly to L3 vertebra inferiorly • The right kidney lies slightly lower than the left kidney because of the large size of the right lobe of the liver. • With contraction of the diaphragm during respiration, both kidneys move downward in a vertical direction by as much as 1 in. (2.5 cm)

Color, Shape & Dimensions of the kidneys • The Kidneys are reddish brown bean-shaped organs with the dimensions of 12 x 6 x 3cm • Although they are similar in size and shape, the left kidney is a longer and more slender organ than the right kidney, and nearer to the midline. • Each kidneys has: • Convex upper & lower ends • A convex lateral border • A medial border that has a vertical slit called the hilum • Internally the hilum extends into a large cavity called the renal sinus.

Hilum & Renal sinus • The hilum transmits, from the front backward, the renal vein, renal artery & the ureter (VAU) • Lymph vessels and sympathetic fibers also pass through the hilum. • The renal sinus contains the upper expanded part of the ureter called the Renal pelvis • Perinephric fat continues into the hilum and sinus and surrounds all structures.

Coverings Fibrous capsule: Surrounds the kidney and is closely applied to the outer surface. Perirenal fat: covers the fibrous capsule Renal (Perirenal) fascia: Condensation of connective tissue that lies outside the perirenal fat and encloses the kidney and the suprarenal gland Pararenal fat: Lies external to the renal fascia, is part of the retroperitoneal fat Structures 2,3 & 4 support the kidneys and hold them in position on the posterior abdominal wall.

Relations The posterior surface of the right and left kidneys are related to similar structures The anterior surface of the both kidneys are related to numerous structures, that are different on both sides. some of these structures have an intervening layer of peritoneum and some lie directlyagainst the surface of the kidney.

Relations:Anterior • Left kidney • a small part of the superior pole, on its medial side, is covered by the left suprarenal gland • the rest of the superior pole is covered by the intraperitoneal stomach and spleen • moving inferiorly, the retroperitoneal pancreas covers the middle part of the kidney; • on its lateral side, the lower half of the kidney is covered by the left colic flexure and the beginning of the descending colon, and, • on its medial side, by the parts of the intraperitoneal jejunum.

Relations: Anterior • Right kidney • a small part of the superior pole is covered by the right suprarenal gland • moving inferiorly, a large part of the rest of the upper part of the anterior surface is against the liver and is separated from it by a layer of peritoneum • medially, the descending part of the duodenum is retroperitoneal and contacts the kidney; • the inferior pole of the kidney, on its lateral side, is directly associated with the right colic flexure and, on its medial side, is covered by a segment of the intraperitoneal small intestine.

Relations:Posterior Common to both kidneys • Diaphragm • Costodiaphragmatic recess, of the pleura • Psoas, quadratuslumborum, transversusabdominis muscles • Subcostal (T12), ilio-hypogastric & ilio-inguinal nerves Difference • As the left kidney lies at higher level than the right, it is related to 11th & 12th ribs and the last intercostal space. • The right kidney is related to 12th rib and the last intercostal space.

Vertebrocostal & Renal Angles • Renal angle: The angle between the last rib and the lateral border of erector spinae muscle, is occupied by kidney • Vertebrocostal angle: The angle between the last rib and the lateral border of vertebral column , is occupied by lower part of the pleural sac. Erector spinae Vertebrocostal angle Renal angle

Internal structure • Each kidney consists of an outer renal cortex and an inner renal medulla. • The renal cortex is a continuous band of pale tissue that completely surrounds the renal medulla. • Extensions of the renal cortex, the renal columns project into the inner aspect of the kidney, dividing the renal medulla into discontinuous aggregations of triangular-shaped tissue, the renal pyramids.

The bases of the renal pyramids are directed outward, toward the renal cortex, while the apex of each renal pyramid projects inward, toward the renal sinus. The apical projection (renal papilla) is surrounded by a minor calyx In the renal sinus, several minor calices unite to form a major calyx, and two or three major calices unite to form the renal pelvis, which is the funnel-shaped superior end of the ureters.

Arterial Supply Lobar arteries Interlobar arteries • The renal artery arises from the aorta at the level of the second lumbar vertebra. • Each renal artery divides into 5 segmental arteries that enter the hilum of the kidney, 4 in front of and one behind the renal pelvis. They are distributed to the different segments of the kidney. • Each segmental artery gives rise to number of lobar arteries, each supplies a renal pyramid. • Before entering the renal substance, each lobar artery gives off two or three interlobar arteries Segmental arteries

Arcuate arteries Interlobar arteries Interlobular arteries • The interlobar arteries run toward the cortex on each side of the renal pyramid. • At the junction of the cortex and the medulla, the interlobar arteries give off the arcuate arteries, which arch over the bases of the pyramids. • The arcuate arteries give off several interlobular arteries that ascend in the cortex and give off the afferent glomerular arterioles.

Segmental branches & • vascular segments of kidneys 1 3 5 • Each kidney has 5 segmental branches and is divided into 5 vascular segments: • Apical • Caudal • Anterior Superior • Anterior Inferior • Posterior 4 2 1 3 5 4 2

Blood Supply Glomerulus

Venous Drainage • Both renal veins drain to the inferior vena cava. The left renal vein enters the inferior vena cava a little above the right vein. The left renal vein: • Is three times longer than the right (7.5 cm and 2.5 cm). So, for this reason the left kidney is the preferred side for live donor nephrectomy. • Course: Runsfrom its origin in the renal hilum: • Posterior to the splenic vein and the body of pancreas, and • Then across the anterior aspect of the aorta, just below the origin of the superior mesenteric artery. • Tributaries: • Left gonadal vein enters it from below • Left suprarenal vein, usually receiving one of the left inferior phrenic veins, enters it above but nearer the midline. • The right renal vein: • Lies behind the 2nd part of the duodenum and sometimes the lateral part of the head of the pancreas

Lymphatic Drainage & Nerve Supply Nerve Supply The nerve supply is the renal sympathetic plexus. The afferent fibers that travel through the renal plexus enter the spinal cord in the T10-12 nerves. Lymphatic Drainage The lymph vessels follow the arteries. Lymph drains to the lateral aortic lymph nodes around the origin of the renal artery.

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The Kidney. David, Sterling, Chelsea &amp; Yuki. Structure. The Beautiful Structure of the KIDNEY. Nephrons. For remembrance purposes; “Zac Nephrons”. What are Nephrons? Nephrons are tiny tubules within the kidney that produce filtrate from the blood and remove waste products as urine.

495 views • 21 slides

Kidney - External Macro Anatomy

Kidney - External Macro Anatomy. Kidney Anatomy. Cortex. Column. Medulla. Base. Papillae. Kidney - Internal Macro Anatomy. Renal Corpuscle. Renal Tubule. Nephron. Renal Corpuscle. Renal corpuscle Site of fluid filtration 2 components glomerulus group of capillary loops

1.85k views • 25 slides

the kidney. functions in waste removal and water/salt balance the funtional unit is the nephron there are about 1 million nephrons in each kidney each nephron has it's own blood supply (to pick up wastes and water) and its own twisted tubule to release the wastes

325 views • 13 slides

Functions of the Kidney

Functions of the Kidney. Maintain electrolyte, acid-base balance “clear” the blood of toxins Make EPO, active Vitamin D gluconeogenesis, hormone metabolism. Hyponatremia Hypokalemia Metabolic Alkalosis chloride responsive chloride unresponsive Metabolic Acidosis anion gap non-anion gap.

601 views • 40 slides

Anatomy of The Kidney. Objectives. By the end of the lecture, the student should be able to describe the : Anatomical features of the kidneys : position, extent, relations, hilum, peritoneal coverings. Internal structure of the kidneys : Cortex, medulla and renal sinus.

1.58k views • 19 slides

KIDNEY RLO 1 – anatomy

KIDNEY RLO 1 – anatomy. Page 1. Kidney gross anatomy. Inferior vena cava.

140 views • 6 slides

Diseases of the Kidney

Diseases of the Kidney. Kidney Physiology Kidney Functions: • activate vitamin D (renal 1-alpha hydroxylase) • produces erythropoietin which stimulates RBC formation • helps regulate blood pressure • ELIMINATES METABOLIC WASTE PRODUCTS • HELPS MAINTAIN FLUID, ELECTROLYTE,

204 views • 16 slides

310 views • 19 slides

The Kidney. Kidney Functions. Filter 200 liters of blood daily, allowing toxins, metabolic wastes, and excess ions to leave the body in urine Regulate volume and chemical makeup of the blood Maintain the proper balance between water and salts, and acids and bases. Other Renal Functions.

536 views • 51 slides

Anatomy of Kidney. By Prof. Saeed Abuel Makarem. Objectives. By the end of the lecture, the student should be able to describe the : Anatomical features of the kidneys: position, extent, relations, hilum, peritoneal coverings. Internal structure of the kidneys :

961 views • 20 slides

Anatomy of the Kidney

Renal Cortex Outer layer Renal Medulla Cone shaped tissue called renal pyramids Renal Pelvis Calyxes cup-shaped tubes Central cavity that is continuous with ureter. Anatomy of the Kidney. Kidney is composed of millions of NEPHRONS Functional unit of kidney

443 views • 14 slides

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Kidneys are those two organs that look like beans which are in charge of removing toxins, controlling several fluids and, well, generating urine. These are very important functions, so any disease that affects these organs can result in severe consequences. Promote your nephrology clinic so that patients put their trust in you. Use these purple slides, which contain some floral decorations, to detail your services, explain the milestones reached, your innovations in the field of medicine, the location of your center, and any other important information.

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The NKF Launches New Online Educational Tool for People Living with CKD

(Sept. 4, 2024, New York, NY) – Today, the National Kidney Foundation (NKF) launched NKF Patient Journey: Chronic Kidney Disease , a new interactive, online learning tool that allows people living with chronic kidney disease (CKD) , to learn more about kidney disease based on their individual health status. This interactive learning experience offers content in a dynamic and engaging way. An initial online survey encourages people to answer questions regarding their health and receive information tailored to their particular stage of kidney disease and what they need to do to manage their CKD and achieve optimal kidney health. Financial support for this educational tool was provided by Novartis Pharmaceuticals Corporation (Novartis).

This innovative tool offers various essential learning journeys – CKD stages 1-5 , dialysis , and kidney transplantation and addresses conditions related to CKD, including pre-diabetes , diabetes , high blood pressure , heart disease , and obesity . To tailor a learner’s journey, this tool captures information about each learner’s kidney health, such as whether they have been told they have CKD, what laboratory data they have available about their kidney health (i.e., serum creatinine with estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR), etc. ) and whether they have any co-morbidities (i.e., pre-diabetes, diabetes, high blood pressure, heart disease, and obesity). People who are unsure if they have CKD are given basic information about CKD and questions to ask their healthcare team.

This learning experience features cloud-based responsive learning. The learning journey branches into different paths based on each learner's responses incorporating text, graphics, videos, and other visuals into manageable segments that allow the learner to focus on a particular topic or subtopic. The online learning tool also includes links to other NKF resources, so the learner can explore specific aspects of living with CKD.

This interactive, curated educational tool is a great first step in dealing with a CKD diagnosis. You can find more information about NKF Patient Journey: Chronic Kidney Disease here: kidney.org/ckd-journey .

“NKF Patient Journey: Chronic Kidney Disease was developed for adult learners because there are many obstacles to patient education that arise not only in primary care but also in specialty care settings,” said Dr. Joseph Vassalotti, NKF Chief Medical Officer. “This innovative tool offers those living with CKD at varying levels of health literacy the individualized health information they need to navigate their kidney health journey. People living with kidney diseases want to know what kidney disease means and what can be done to improve kidney health on an individualized basis.”

Many people rely on information found online to help them better understand the health information their clinician told them about during their last office visit. NKF Patient Journey: Chronic Kidney Disease will help people living with CKD filter through the volumes of information available on the internet based on their particular kidney health journey. Having comprehensive, evidence-based, freely available resources that guide people through essential information is a benefit to busy clinicians. Information provided in an easy-to-understand format helps patients understand what they can do today to take better control of their kidney health.

“Learning you have kidney disease is oftentimes frightening and frustrating because there is a lot of new information to parse through; those living with CKD need information that is understandable and actionable,” said Kevin Longino, NKF Chief Executive Officer and a kidney transplant recipient. “NKF Patient Journey: Chronic Kidney Disease was created for those who might be overwhelmed by their diagnosis and all the information on the internet, doctor visits, and social media forums. NKF is committed to being a credible source of information for every person living with kidney disease, or a kidney transplant, so they can make informed decisions about their particular stage and type of kidney disease.”

CKD is a widely unrecognized public health crisis affecting an estimated 35.5 million U.S. adults among whom approximately 90% of those don’t even know they have it. About 1 in 3 adults in the U.S. (approximately 80 million) are at risk for kidney disease. Kidney disease is considered a silent killer so people with certain risk factors like diabetes , high blood pressure , heart disease , obesity , and a family history of kidney disease , gout , or hyperkalemia (high potassium) are all at risk for kidney disease and will all benefit from utilizing this educational tool and learning more about their overall kidney health.

For more information about NKF Patient Journey: Chronic Kidney Disease, please visit kidney.org/ckd-journey and for more details about CKD or kidney disease, visit kidney.org .

About Kidney Disease

In the United States, 35.5 million adults are estimated to have chronic kidney disease —and approximately 90% don’t know they have it. About 1 in 3 American adults are at risk for chronic kidney disease. Risk factors for kidney disease include: diabetes , high blood pressure , heart disease , obesity , and family history of kidney disease . People of African American, Hispanic, American Indian, Asian, or Pacific Islander descent are at increased risk for developing the disease. African Americans are almost 4 times more likely than White Americans to have kidney failure. Hispanics are 1.3 times more likely than non-Hispanics to have kidney failure.

About Kidney Equity For All

Historically, access to kidney health has remained inequitable, with persistent disparities disproportionately affecting underserved populations and impacting the entire kidney patient journey. To address these disparities, NKF is urging industry and community leaders to join them on their KIDNEY EQUITY FOR ALL"™ "mission by allocating resources to improve healthcare access and outcomes in communities of color. This is a tangible opportunity for businesses to incorporate Environmental, Social and Governance (ESG) principles into their operations. For more information on KIDNEY EQUITY FOR ALL™, visit www.kidneyequityforall.org .

About The National Kidney Foundation

The National Kidney Foundation is the largest patient-centric organization dedicated to the awareness, prevention, and treatment of kidney disease in the U.S. It is revolutionizing the fight to save lives by eliminating preventable kidney disease, accelerating innovation for the dignity of the patient experience, and dismantling structural inequities in kidney care, dialysis, and transplantation. For more information about NKF, please visit www.kidney.org .

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Liver and Kidney Tumor Masses as the Initial Presentation of B-Cell Acute Lymphoblastic Leukemia

Affiliation.

• 1 From the Ganzhou Institute of Medical Imaging, Ganzhou Key Laboratory of Medical Imaging and Artificial Intelligence, Medical Imaging Center, Ganzhou People's Hospital, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou, Jiangxi, China.
• PMID: 39235153
• DOI: 10.1097/RLU.0000000000005428

We described a 13-year-old girl who presented unexplained paroxysmal sharp pain in the right upper abdomen for 3 days. CT and MRI showed multiple masses in the liver and kidneys, initially diagnosed as lymphoma. The hepatic mass biopsy confirmed B-cell lymphoblastic lymphoma. FDG PET/CT examination found that the liver and kidney masses demonstrated high metabolic activity, with concomitant increased metabolic activity in the skeleton. Bone marrow biopsy revealed extensive skeletal involvement. The final diagnosis was B-cell acute lymphoblastic leukemia. This case highlights the effectiveness of FDG PET/CT as an adjunct imaging modality for diagnosis.

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Conflict of interest statement

Conflicts of interest and sources of funding: none declared. This research was funded in whole, or in part, by the National Natural Science Foundation of China (grant number 82160330), the Jiangxi Provincial Natural Science Foundation (grant number 20202ACBL216006), and the Ganzhou Health Commission Scientific Research Planning Project (grant number GZWJW202402108).

• Cortelazzo S, Ferreri A, Hoelzer D, et al. Lymphoblastic lymphoma. Crit Rev Oncol Hematol. 2017;113:304–317.
• Hoelzer D, Gökbuget N. T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity? Clin Lymphoma Myeloma. 2009;9:S214–S221.
• Raetz EA, Perkins SL, Bhojwani D, et al. Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Pediatr Blood Cancer. 2006;47:130–140.
• Cistaro A, La Delfa V, Di Rosa G, et al. MRI and 18F-FDG-PET/CT in a rare case of early (precursor) B-lymphoblastic leukaemia with bone involvement as initial manifestation. Nucl Med Rev. 2017;20:57–59.
• Loghavi S, Kutok JL, Jorgensen JL. B-acute lymphoblastic leukemia/lymphoblastic lymphoma. Am J Clin Pathol. 2015;144:393–410.

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