Procedure Practice 05/15/00 - Coding Recommendations

Feature Article 05/15/00

The Urologic System - Part 1:
The Kidneys

Structure - Function - Common Diseases - Dialysis - Coding Tips/Guidelines
  

Diseases of the kidneys and urinary tract are a major cause of illness and death in the United States. Over 3.5 million people have diagnosed kidney disorders, and an additional 8 million people each year suffer from a variety of acute urologic system problems. The urologic system includes the kidneys, ureters, urinary bladder, and urethra. Over the next two months we will review the structure and function of these organs and the diseases affecting them, learn about some of the associated diagnostic and therapeutic procedures, and discuss urologic coding issues. We begin with the kidneys, the major organs of the system. Next month, we will cover the ureters, bladder, and urthra of the lower urinary tract.

Structure

The kidneys are paired organs located retroperitoneally in the lumbar area. The right kidney lies somewhat lower than the left because of displacement by the liver. The left kidney is slightly longer than the right and lies closer to the midline. The kidneys assume different locations depending upon the body’s position, and they move up and down during expiration and inspiration with the motion of the diaphragm. Connective tissues (the renal fasciae) anchor the kidneys to surrounding structures and help maintain their normal position.

The kidneys have a bean shape in which one side is convex and the other is concave. Normal adult kidneys are about 10 to 13 cm long, 5 to 7.5 cm wide, and each is encased in a protective transparent, fibrous membrane called the renal capsule. The concave part of the kidney attaches to two of the body's crucial blood vessels-the renal artery and the renal vein-and the ureter, a tubelike structure that carries urine to the bladder.

The cortex is the outmost layer. Beneath the cortex lies the medulla, an area that contains between 8 and 18 cone-shaped sections known as pyramids, which are formed almost entirely of bundles of microscopic tubules. The tips of these pyramids point toward the center of the kidney. At the center of the kidney is a cavity called the renal pelvis. The pelvic calices (sing. calyx) are flower-shaped branches of the pelvis that extend between the pyramids.

The task of filtering the blood is performed by millions of nephrons, structures that extend between the cortex and the medulla. Under magnification, nephrons look like tangles of tiny vessels or tubules, but each nephron has an orderly arrangement that makes filtration of wastes from the blood possible. The primary structure in this filtering system is a network of capillaries called the glomerulus. The glomerulus sits in a cuplike structure called Bowman's capsule, from which extends a narrow vessel called the renal tubule. This tube twists and turns until it drains into a collecting tubule that carries urine toward the renal pelvis. Part of the renal tubule, called Henle's loop, becomes extremely narrow, extending down away from Bowman's capsule and then back up again in a U shape. Surrounding Henle's loop and the other parts of the renal tubule is a network of capillaries formed from a small blood vessel that branches out from the glomerulus.

Function

The kidneys remove poisonous wastes from the blood. Chief among these wastes are the nitrogen-containing compounds urea and uric acid, which result from the breakdown of proteins and nucleic acids. Life-threatening illnesses occur when too many of these waste products accumulate in the blood.

Blood enters the kidneys through the renal artery. The artery divides into smaller and smaller arterioles, eventually ending in the tiny capillaries of the glomerulus. The capillary walls here are very thin and the blood pressure within the capillaries is high. The result is that water and any substances dissolved in it such as salts, glucose, amino acids, and the waste products urea and uric acid, are pushed out through the thin capillary walls, to be collected in Bowman's capsule. Larger particles in the blood, such as red blood cells and protein molecules, are too bulky to pass through the capillary walls and they remain in the blood. The filtered blood leaves the glomerulus through another arteriole that branches into the meshlike network of blood vessels around the renal tubule. The blood then exits the kidneys through the renal vein. Approximately 180 liters (about 50 gallons) of blood moves through the two kidneys every day.

Urine production begins with the water, salts, and other substances collected by the glomerulus in Bowman’s capsule as blood passes through the kidneys. This liquid, called glomerular filtrate, moves from Bowman's capsule through the renal tubule. As the filtrate flows through the renal tubule, the network of blood vessels surrounding the tubule reabsorbs much of the water, salt, and virtually all of the nutrients, especially glucose and amino acids, that were removed in the glomerulus. This important process, called tubular reabsorption, enables the body to selectively keep the substances it needs while ridding itself of wastes. Eventually, about 99 percent of the water, salt, and other nutrients is reabsorbed.

At the same time that the kidneys reabsorb valuable nutrients from the glomerular filtrate, they carry out an opposing task called tubular secretion. In this process, unwanted substances from the capillaries surrounding the nephron are added to the glomerular filtrate. These substances include various charged particles called ions, including ammonium, hydrogen, and potassium ions.

Together, glomerular filtration, tubular reabsorption, and tubular secretion produce urine, which flows into collecting ducts and into the microtubules of the pyramids. The urine is then stored in the renal pelvis and eventually drained into the ureters.

In addition to filtering the blood, the kidneys perform several other essential functions. One such activity is regulation of the amount of water contained in the blood. This process is influenced by antidiuretic hormone (ADH), also called vasopressin, which is produced in the hypothalamus and stored in the nearby pituitary gland. Receptors in the brain monitor the blood's water concentration. When the amount of salt and other substances in the blood becomes too high, the pituitary gland releases ADH into the bloodstream. When it enters the kidneys, ADH makes the walls of the renal tubules and collecting ducts more permeable to water so that more water is reabsorbed into the bloodstream.

The hormone aldosterone, produced by the adrenal glands, interacts with the kidneys to regulate the blood's sodium and potassium content. High amounts of aldosterone cause the nephrons to reabsorb more sodium ions, more water, and fewer potassium ions; low levels of aldosterone have the reverse effect. The kidneys’ responses to aldosterone help keep the blood's salt levels within the narrow range that is best for crucial physiological activities.

Aldosterone also helps regulate blood pressure. When blood pressure starts to fall, the kidneys release an enzyme called renin, which converts a blood protein into the hormone angiotensin. This hormone causes blood vessels to constrict, resulting in a rise in blood pressure. Angiotensin then induces the adrenal glands to release aldosterone, which promotes sodium and water reabsorption to further increase blood volume and blood pressure.

The kidneys also adjust the body's acid-base balance to prevent such blood disorders as acidosis and alkalosis, both of which impair the functioning of the central nervous system. If the blood is too acidic, meaning that there is an excess of hydrogen ions, the kidneys move these ions to the urine through the process of tubular secretion. The kidneys also process vitamin D, converting it to an active form that stimulates bone development.

The kidneys also produce several hormones. One of these, erythropoietin, influences the production of red blood cells in the bone marrow. When the kidneys detect that the number of red blood cells in the body is declining, they secrete erythropoietin. This hormone travels in the bloodstream to the bone marrow, stimulating the production and release of more red cells.

Common Kidney Diseases

 
Pyelonephritis, an inflammation of the kidney, is the most common form of kidney disease. Most cases are caused by a bacterial infection that starts in the bladder and spreads to the kidney. Sometimes an obstruction that interferes with the flow of urine in the urinary tract can cause the disease. Symptoms of pyelonephritis include fever, chills, and back pain.
 

Glomerulonephritis, another common kidney disease, is characterized by inflammation of some of the kidney's glomeruli. The condition may be acute or chronic. Usually it occurs when the body's immune system is impaired and is often a late complication of pharyngitis or skin infection. Antibodies and other substances form large particles in the bloodstream that become trapped in the glomeruli. These trapped particles cause inflammation and prevent the glomeruli from working properly. Symptoms may include blood in the urine, swelling of body tissues, and the presence of protein in the urine in laboratory tests. If acute glomerulonephritis does not resolve within one or two years, or if it progressed to chronic renal failure or chronic renal insufficiency, it is considered chronic glomerulonephritis.
  

Diabetic nephropathy is one of the most serious complications of diabetes mellitus. After years of diabetes, the glomeruli become scarred and do not filter blood efficiently. High blood pressure and elevated blood glucose are two of the factors that contribute to glomerular damage. Eventually the kidneys may fail completely so that dialysis or transplant is necessary.
  

Nephrolithiasis is the presence of urinary calculi within the kidney. Stones may form because the urine becomes too saturated with salts or because the urine lacks the normal inhibitors of stone formation. About 80 percent of the stones are composed of calcium; the remaining 20% consist of various substances, including uric acid, cystine, and struvite. Struvite stones, a mixture of magnesium, ammonium, and phosphate, are also called infection stones because they form only in infected urine. Stones vary in size from too small to be seen with the eye alone to 1 inch or more in diameter. A large staghorn calculus may be shaped by and may fill almost the entire renal pelvis and calices.

Tiny stones may not cause any symptoms. Stones that obstruct the ureter or renal pelvis or any of its drainage calices may cause back pain or renal colic. Other symptoms include nausea and vomiting, abdominal distention, chills, fever, and hematuria. Urinary frequency often occurs as the stone makes its way down the ureter.

If stones block the flow of urine, bacteria become trapped in urine that pools above the blockage, leading to an infection. If stones block the urinary tract for a long time, urine backs up in the renal calices producing pressure that can distend the kidneys (hydronephrosis) and eventually damage them.

 
Hydronephrosis is distention of the kidney with urine caused by backward pressure on the kidney when the flow of urine is obstructed. Normally, urine flows out of the kidneys at extremely low pressure. If the urine flow is obstructed, urine backs up in the small tubes of the kidney and the central collecting area (renal pelvis), distending the kidney and putting pressure on its tissues. The pressure from prolonged and severe hydronephrosis ultimately damages the kidney's tissues so that kidney function is gradually lost. Hydronephrosis commonly results from ureteropelvic junction (UPJ) obstruction (an obstruction where the ureter and renal pelvis meet). Obstruction may be due to:

• Structural abnormalities
   
• Kinking of the ureter at the UPJ
   
• Stones in the renal pelvis
   
• Compression of the ureter by an abnormally located blood vessel or tumor
   

Hydronephrosis can also result from an obstruction below the junction of the ureter and renal Pelvis or from backflow of urine from the bladder

 
Acute renal failure (ARF) is a rapid decline in the kidneys' ability to clear the blood of toxic substances, leading to an accumulation of metabolic waste products, such as urea, in the blood. Acute kidney failure can result from any condition that decreases the blood supply to the kidneys (prerenal failure), obstructs the flow of urine after it has left the kidneys (postrenal failure), or injures the kidneys themselves (intrinsic failure). Toxic substances may damage the kidneys. Such toxic substances include drugs, poisons, crystals precipitated in the urine, and antibodies that react against the kidneys. Symptoms depend on the severity of kidney failure, its rate of progression, and its underlying cause.
 

Chronic renal failure (CRF) is a slowly progressive decline in kidney function that leads to azotemia, a buildup of metabolic waste products in the blood. Chronic kidney failure is caused by many diseases, including the following:

• Primary hypertension
  
• Urinary tract obstruction
  
• Glomerulonephritis
  
• Kidney abnormalities such as polycystic kidney disease
  
• Diabetes mellitus
  
• Autoimmune disorders such as systemic lupus erythematosus

All of these diseases are chronic, progressive conditions. End-stage renal disease is a progression of CRF to the point at which chronic maintenance dialysis or kidney transplantation is required to keep the patient alive.
 

Kidney cancer (adenocarcinoma of the kidney; renal cell carcinoma; hypernephroma) accounts for about 2 percent of cancers in adults, affecting one and a half times as many men as women. Cancer can occur in the cells lining, the renal pelvis (transitional cell carcinoma of the renal pelvis), and the ureters.

 
Polycystic kidney disease is a hereditary disorder in which many cysts form in both kidneys; the kidneys grow larger but have less functioning kidney tissue. The genetic defect that causes polycystic kidney disease may be dominant or recessive. A person with the disease has inherited either a dominant gene from one parent or two recessive genes, one from each parent. Those with dominant gene inheritance usually have no symptoms until adulthood; those with recessive gene inheritance have severe illness in childhood.

In children, polycystic kidney disease causes the kidneys to become very large and the abdomen to protrude. A severely affected newborn may die shortly after birth, because kidney failure in the fetus leads to poor development of the lungs. The liver is also affected, and at 5 to 10 years of age, a child with this disorder tends to develop portal hypertension. Eventually liver failure and kidney failure occur. In adults, polycystic kidney disease progresses slowly over many years. Symptoms usually include back pain, hematuria, urinary tract infections, oliguria, and renal colic.
 

Renal tubular acidosis is a disorder in which the kidney tubules can't adequately remove acid from the blood to excrete into the urine. Renal tubular acidosis may be hereditary or may be caused by drugs, heavy metal poisoning, or an autoimmune disease, such as systemic lupus erythematosus or Sjögren's syndrome. Healthy kidneys remove acid from the blood and excrete it into the urine. In renal tubular acidosis, the tubules malfunction and insufficient amounts of acid are excreted into the urine. As a result, acid builds up in the blood, a condition called metabolic acidosis. Metabolic acidosis may lead to hypokalemia, calcium deposits in the kidneys, dehydration, and osteomalacia.
 

Nephrogenic diabetes insipidus is a disorder in which the kidneys produce a large volume of dilute urine because they fail to respond to antidiuretic hormone and are unable to concentrate urine. Nephrogenic diabetes insipidus may be hereditary. The gene that causes the disorder is recessive and carried on the X chromosome, so usually only males develop symptoms. However, females who carry the defective gene can transmit the disease to their sons. Other causes of nephrogenic diabetes insipidus include the use of drugs that can damage the kidneys. Such drugs include aminoglycoside antibiotics; demeclocycline, another antibiotic; and lithium.

If nephrogenic diabetes insipidus is hereditary, the primary symptoms of polydipsia and polyuria usually start soon after birth. Infants may become severely dehydrated, develop a high fever, vomit, or suffer seizures. If their disease isn't quickly diagnosed and treated, the brain may be damaged, leaving the infant with permanent mental retardation. Frequent episodes of dehydration can also retard physical development.
 

Nephrotic syndrome is not a separate disease, but a collection of symptoms caused by many diseases that affect the kidneys, resulting in severe, prolonged loss of protein into the urine, decreased  levels of protein in the blood, retention of excess salt and water in the body, and increased levels of fats (lipids) in the blood. The condition can occur at any age. The diagnosis of nephrotic syndrome is based on symptoms and laboratory findings. Laboratory tests of urine detect high levels of protein with clumps of cells (casts). The blood concentration of albumin is low because this vital protein is lost in the urine and its synthesis is impaired. Urine levels of sodium are low and levels of potassium are high.
 

Horseshoe kidney is the most common congenital anomaly of kidney formation. The kidneys are joined with an isthmus of tissue across the midline. The ureters run medially and anteriorly over this isthmus and generally drain well. However, obstruction of urinary flow may occur secondary to an abnormally high insertion site of the ureter into the renal pelvis.
 

Medullary sponge kidney is a congenital dilatation of the renal collecting ducts due to tubular ectasia or dysplasia in the pericalyceal region of the renal pyramids. The kidney tissue has a sponge-like appearance. Usually this condition has no symptoms; however, the abnormal texture of the kidney causes urinary stasis. People with this disorder may suffer recurrent urinary tract infections, hematuria, and renal calculi.
 

Blood vessel disorders of the kidneys can damage the kidneys, impair their function, and increase blood pressure.
 

Renal infarction is the death of an area of kidney tissue caused by a blockage of the renal artery, the main artery that carries blood to the kidney. Blockage of the renal artery is rare, most frequently resulting from an embolus lodging in the artery. The embolus may originate from a thrombus in the heart or from the breakup of a cholesterol deposit in the aorta. Alternatively, the infarction may result from the formation of a blood clot (acute thrombosis) in the renal artery itself due to arterial injury. The clot may also result from severe atherosclerosis, arteritis sickle cell disease, or the rupture of a renal artery aneurysm. A tear in the lining (acute dissection) of the renal artery causes blood flow in the artery to be blocked or the artery to rupture.
 

Atheroembolic kidney disease is a condition in which numerous small emboli clog the small renal arteries with resultant kidney failure. Tiny atheromatous placques lodged on a blood vessel wall break off, travel to the small renal arteries, and become trapped. This condition may occur spontaneously or as a complication of surgery or procedures affecting the aorta, such as angiography, in which pieces of atheromatous placques lining the aorta are unintentionally dislodged. Atheroembolic kidney disease occurs most commonly in elderly people and the risk increases with age.
 

Renal arteriosclerosis (benign nephrosclerosis) commonly accompanies aging and is associated with high blood pressure. Malignant nephrosclerosis is a much more severe condition that occurs with hypertensive renal disease when the hypertension becomes accelerated or malignant. Malignant hypertension most commonly results from poorly controlled high blood pressure but may result from other conditions, such as glomerulonephritis, chronic kidney failure, narrowing of the renal artery (renal vascular hypertension), inflammation of kidney blood vessels (renal vasculitis), or, rarely, hormonal disorders such as pheochromocytoma or Cushing's syndrome.

Dialysis Treatment

Patients with end-stage renal disease require dialysis in order to manage symptoms arising from their chronic renal failure. Several dialysis techniques exist.
 

Hemodialysis is a procedure in which the blood is removed from the body and circulated through a machine outside the body called a dialyzer, requiring repeated access to the bloodstream. An artificial connection between an artery and a vein (an arteriovenous fistula) is made surgically to facilitate that access. In hemodialysis, blood flows through a tube connected to the arteriovenous (A-V) fistula and is pumped to the dialyzer. Heparin is used during dialysis to prevent blood from clotting in the dialyzer. Inside the dialyzer, a porous artificial membrane separates the blood from a fluid (the dialysate) that is similar in chemical composition to normal body fluids. Pressure in the dialysate compartment of the membrane unit is lower than in the blood compartment, allowing fluid, waste products, and toxic substances in the blood to filter through the membrane into the dialysate. However, blood cells and large proteins are too large to filter through the small pores of the membrane. The dialyzed (purified) blood is returned to the person's body. Dialyzers have different sizes and degrees of efficiency. Newer units are very efficient, allowing blood to flow faster and shortening dialysis time--for example, 2 to 3 hours three times a week compared to 3 to 5 hours three times a week with an older unit. Most people who have chronic kidney failure need hemodialysis three times a week to remain healthy.
 

Peritoneal dialysis uses the peritoneum, the membrane lining the abdomen and abdominal organs, as a permeable filter. This membrane has a large surface area and a rich network of blood vessels. Substances from the blood can easily filter through the peritoneum into the abdominal cavity if conditions are right. Fluid is infused through a catheter inserted through the abdominal wall into the peritoneal space within the abdomen. The fluid must be left in the abdomen for a sufficient time to allow waste materials from the bloodstream to pass slowly into it. Then the fluid is drained out, discarded, and replaced with fresh fluid. A soft silicone rubber or porous polyurethane catheter is usually used because it allows the fluid to flow smoothly and is unlikely to cause damage. A catheter can be put in place temporarily or it may be put in place permanently in an operating room. One type of permanent catheter eventually forms a seal with the skin and can be capped when not in use.

Various techniques are used for peritoneal dialysis. In the simplest technique, manual intermittent peritoneal dialysis, bags containing fluid are warmed to body temperature. The fluid is infused into the peritoneal cavity for 10 minutes, allowed to remain there for 60 to 90 minutes, and then drained in about 10 to 20 minutes. The entire treatment can take 12 hours. This technique is used chiefly to treat acute kidney failure.

Automated cycler intermittent peritoneal dialysis can be performed by people at home, eliminating the need for constant nursing attention. A timed device automatically pumps fluid into and drains it from the peritoneal cavity. Usually, people set the cycler at bedtime so the dialysis takes place while they're sleeping. These treatments need to be performed 6 or 7 nights a week.

In continuous ambulatory peritoneal dialysis the fluid is kept in the abdomen for extremely long intervals. Typically, the fluid is drained and replenished four or five times a day. The fluids are packaged in collapsible vinyl bags that can be folded when empty and used for subsequent drainage without being disconnected from the catheter. People generally perform three of these fluid exchanges during the day, at intervals of 4 hours or longer. Each exchange takes 30 to 45 minutes. A longer exchange (8 to 12 hours) is performed at night, during sleep.

Another technique, continuous cycler-assisted peritoneal dialysis, uses an automated cycler to perform short exchanges at night during sleep, whereas longer exchanges are performed without the cycler during the day. This technique minimizes the number of exchanges during the day but prevents mobility at night because of cumbersome equipment.

Coding Tips and Guidelines

	Kidney conditions are assigned codes from the 580 through 593.9 range in ICD-9-CM Chapter 10, "Genitourinary System." However, depending upon the etiology of the kidney disease, it may be necessary to assign codes from other chapters. For example, some infectious diseases affecting the kidney are classified to Chapter 1. Renal trauma is coded to Chapter 17. Acute renal failure following labor and delivery is assigned a code from Chapter 11. Be sure to read all inclusion, exclusion, and instructional notes that accompany each code.
	Codes in the 580 subcategory refer to acute glomerulonephritis only. If acute glomerulonephritis has advanced to chronic renal insufficiency or CRF, the condition is no longer acute. Assign a code from the 582 series instead.
	An acute exacerbation of chronic glomerulonephritis is coded to category 582 alone. Do not assign an additional code from subcategory 580. Remember, the acute phase of the condition no longer exists.
	Refer to the ICD-9-CM index entry for "Glomerulonephritis, due to or associated with" for a list of etiologic conditions. The index refers to the following codes in italicized brackets: 580.81, 581.81, 582.81, 583.81. These brackets indicate that glomerulonephritis with these conditions is considered a manifestation of the underlying disease and therefore would be sequenced after the code for the etiology. For example, chronic proliferative glomerulonephritis due to or associated with tuberculosis identified by bacterial culture is coded 016.04 and 582.81.
	Nephrotic syndrome is the end point of glomerulonephritis. Therefore, do not code glomerulonephritis in addition to the syndrome.
	Nephrotic syndrome may or may not be present with chronic renal failure. Only code nephrotic syndrome if the condition is documented by the physician.
	Codes for nephritis, nephrotic syndrome, and nephrosis exclude conditions associated with hypertensive renal disease (403.00-403.91).
	Acute renal failure due to trauma is classified to 958.5.
	Acute renal failure following labor and delivery is coded 669.3 with the appropriate 5th digit of 0, 2, or 4.
	Acute renal failure following abortion is coded 639.3.
	If diabetes is the documented cause of renal failure, assign the diabetes code 250.4x with renal failure as an additional diagnosis.
	Assign codes from category 403, Hypertensive renal disease, if chronic renal failure, unspecified renal failure, or nephrosclerosis (conditions in the 585-587 code range) exists in the presence of hypertension. ICD-9-CM presumes a cause and effect relationship if these conditions coexist unless documentation specifically states that this relationship does NOT exist.
	ICD-9-CM does not assume a cause and effect relationship between hypertension and acute renal failure. Select a code from category 584 to correctly identify the ARF.
	Assign codes from combination category 404, Hypertensive heart and renal disease, if both hypertensive renal disease and hypertensive heart disease are documented. Again, ICD-9-CM assumes a relationship between the hypertension and the renal failure whether or not the relationship is specifically stated.
	Admission for dialysis is coded V56.0. Also code the associated condition(s).
	Dialysis disequilibrium syndrome is an electrolyte imbalance. Assign 276.9, Electrolyte and fluid disorders not elsewhere classified. Also assign the appropriate code for the underlying kidney disease and V45.1 to indicate dialysis status.
	Assign V56.0 and V56.1 to code admission for dialysis treatment with flushing of clots from the catheter during the encounter.
	Infection of a peritoneal dialysis catheter is coded 996.68. Also code the kidney disease and the bacterial agent, if known.
	Infection of a vascular access catheter or shunt is coded 996.62. Again, also code the kidney disease and the bacterial agent, if known.

Practice Makes Perfect!

Are you ready for some hands-on practice? Read the patient reports on our Procedure Practice page. Assign the appropriate codes and then compare your answers with our coding recommendations. Good luck!

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