Causes and Symptoms Disorders of the kidney can occur for a variety of reasons. The cause may be congenital (present from birth) or may develop very quickly and at any age. Many of these problems and disorders can be easily treated. The main types of kidney disorder are malformations in the development of the kidney, part of the kidney, or the ureter; glomerular disease; tubular and interstitial disease or disruption; vascular (other than glomerular) disease; and kidney dysfunction that occurs secondary to another disease.
The kidney frequently exhibits congenital anomalies, some of which occur during specific developmental stages. Agenesis occurs when the ureteric bud fails to develop normally. When the tissue does not develop, the ureter itself fails to form. If there is an obstruction where the ureter joins the pelvis of the kidney, there may be massive hydronephrosis (dilation). One or both kidneys may be unusually small, containing too few tubules. The kidneys may be displaced, too high or offset to one side or the other. They may even be fused. All these conditions could seriously affect the manufacture of urine, its excretion, or both.
Glomerulonephritis refers to a diverse group of conditions that share a common feature: primary involvement of the glomerulus. The significance of glomerulonephritis is that it is the most common cause of end-stage renal failure. Its features include urinary casts, high protein levels (proteinuria), hematuria, hypertension, edema (swelling), and uremia. The two forms of glomerulonephritis are primary and secondary. In the primary form, only the kidneys are affected; in the secondary form, the lesion (affected area) is only one of a series of problems.
Nephrotic syndrome
is usually defined as an abnormal condition of the kidney characterized by the presence of proteinuria together with edema and high fat and cholesterol levels. It occurs in glomerular disease, in thrombosis of a renal vein, and as a complication of many systemic diseases. Nephrotic syndrome occurs in a severe, primary form characterized by anorexia, weakness, proteinuria, and edema.
Interstitial nephritis
is inflammation of the interstitial tissue of the kidney, including the kidneys. Acute interstitial nephritis is an immunologic, adverse reaction to certain drugs, especially nonsteroidal anti-inflammatory drugs (NSAIDs) and some antibiotics. Acute renal failure, fever, rash, and proteinuria are indicative signs of this condition. If the medication is stopped, normal kidney function returns. Chronic interstitial nephritis is defined as inflammation and structural changes associated with such conditions as ureteral obstruction, pyelonephritis, exposure of the kidney to a toxin, transplant rejection, and certain systemic diseases.
Kidney stones
(calculi) are commonly manufactured from calcium oxalate or phosphate, triple phosphate, uric acid (urate), or a mixture of these. Calcium stones are not necessarily the result of high serum calcium, although they can be. Struvite calculi of magnesium ammonium (triple) phosphate mixed with calcium are bigger but softer than other types; they grow irregularly, filling much of the kidney pelvis. They arise from infection with urea-splitting organisms that cause alkaline urine. Urate stones are a complication of gout.
Those who have a tendency to develop stones may experience concomitant infection known as pyonephrosis. Pyonephrosis is a result of not only blockage at the junction of the ureter and kidney pelvis but also any constricture at this location. Bacteria from the bloodstream collect and cause an abscess to form. If the tube is completely blocked, the inflammation produces enough pus to rupture a portion of the kidney, and more of the abdominal cavity becomes involved.
Pyelonephritis is inflammation of the upper urinary tract. Acute pyelonephritis may be preceded by lower tract infection. The patient complains of lethargy, fever, and back pain. The major symptoms are fever, renal pain, and body aches, accompanied by nausea and toxemia. Chronic pyelonephritis often affects the renal tubules and the small spaces within the kidney. Fibrous tissue may take over these areas and cause gradual shrinking of the functional kidney. The chronic form may also result from previous bacterial infection, reflux, obstruction, overuse of analgesics, x-rays, and lead poisoning.
Obstruction may be caused by inadequate development of the renal tissue itself, closing off one or both ureters. Other malformations and certain calculi can also obstruct urine flow. Reflux may occur when the contraction of the bladder forces urine backward, up toward and into the kidney. Lesser degrees of reflux do not damage the kidney, but the greater the reflux, the more likely damage will occur. Bacterial infection is often attributable to Escherichia coli, but other bowel bacteria may also infect the area. They generally move upward from outside the body through the urinary organs, but they may also move inward from the bloodstream.
Acute renal failure is defined as a sudden decline in normal renal function that leads to an increase in blood urea and creatinine. The onset may be fast (over days) or slow (over weeks) and is often reversible. It is characterized by oliguria and rapid accumulation of nitrogenous wastes in the blood, resulting in acidosis. Acute renal failure is caused by hemorrhage, trauma, burns, toxic injury to the kidney, acute pyelonephritis or glomerulonephritis, or lower urinary tract obstruction. Occasionally, it will progress into chronic renal failure.
Chronic renal failure may result from many other diseases as well. Its signs are sluggishness, fatigue, and mental dullness. Patients also display other systemic problems as a result of chronic renal failure. Almost all such patients are anemic, and three-fourths of them develop hypertension. The skin becomes discolored, a muddy coloration caused by anemia and the presence of excess melanin.
Renal symptoms suggestive of renal dysfunction include increases in frequency of urination, color changes in urine, areas of edema, and hypertension. The patient may experience only one symptom but is more likely to have a series of complaints. To determine the cause of renal disease, several diagnostic tools can be used to distinguish the type of pathogenic process affecting the kidney. The degree to which other body systems are involved determines whether the disease process is systemic or confined to the kidneys. Other valuable clues may be gathered from medical history, family history, and physical examination. The key factors, however, are renal size and renal histopathology.
Examination of the urine can reveal important data relative to renal health. Stick tests may show the abnormal presence of blood, glucose, or protein. Assaying the kind and amount of protein may pinpoint the cause of the disease. Urine contaminated with bacteria has always been used as an indication of some form of urinary tract infection. Microscopic examination of urine sediment may help diagnose acute renal failure. Blood tests may also indicate the source of a renal disorder. A series of blood tests might reveal rising urea and creatinine levels. The urea-to-creatinine ratio may aid in determining if and which type of acute renal failure may be present. A high red cell count might suggest kidney stones, a tumor, or glomerular disease; a high white cell count would hint at inflammation or infection. Cells cast from the kidney tubules may indicate acute interstitial nephritis, while red cell breakdown products may mean glomerulonephritis. The diagnostician should also be diligent in tracking down possible septic causes. Repeated cultures of blood and urine should help ascertain if there is an abscess anywhere near the kidney.
X-rays can provide useful information. An abdominal x-ray may show urinary stones and abnormalities in the renal outline. Ultrasound will measure renal size, show scarring, and reveal dilation of the tract, perhaps as a result of an obstructive lesion. Abdominal ultrasound has become the investigation of choice because it can be performed at the patient’s bedside.
Renal biopsy can give an accurate diagnosis of acute renal failure but may be more dangerous to the patient than the condition itself. The main indications for biopsy would be suspected acute glomerulonephritis and renal failure that has lasted six weeks.
Treatment and Therapy If glomerulonephritis is suspected or diagnosed, its treatment seeks to avoid complications of the illness. The patient is monitored daily for fluid overload; as long as the patient is retaining fluid, blood tests that measure urea, creatinine, and salt balance are also run daily. The patient should stay in bed and restrict fluid as well as potassium intake. Medications may be prescribed, including diuretics, vasodilators for hypertension, and calcium antagonists. If the cause is bacterial, a course of oral antibiotics may be given. If these measures are unsuccessful, short-term dialysis may be needed. Some urinary abnormalities may last for as long as a year.
The first measure undertaken to treat acute renal failure is to rebuild depressed fluid volumes: blood if the patient has hemorrhaged, plasma for a burn patient, and electrolytes for a patient who is vomiting and has diarrhea. If infection is suspected as the underlying cause, an appropriate antibiotic should be administered when blood cultures confirm the presence of bacteria. After fluid volumes have been replenished, a diuretic may be necessary to reduce swelling of tissues within the kidney.
In chronic renal failure, the major undertaking is to relieve the obstruction of the urinary tract. If the blockage is within the bladder, simple catheterization may relieve it. If a stone or some similar obstacle is blocking a ureter, however, surgery to remove it may be necessary. A tube may be inserted to allow urine drainage, and the stone will pass or be removed.
For those suffering from recurrent
stones, maintaining a high urine output is important; this requires the patient to drink fluids throughout the day and even at bedtime. Patients enduring intense pain may need to be hospitalized. Analgesics for pain are administered, in addition to forced fluid intake to increase urine output so that the stone might be passed. If these measures do not work, surgical intervention may be necessary.
Patients suffering from progressive, incurable renal failure need medical aid in managing conservation of, substitution for, and eventual replacement of nephron function. Conservation attempts to prolong kidney function for as long as possible; renal function is aided by drug treatment. Substitution means the maintenance of kidney function by dialysis, especially hemodialysis. Replacement is the restoration of renal function by a kidney transplant. By this third stage of treatment, urine formation is independent of further drug treatment, and kidney function must be achieved by other means. Patients suffering from end-stage renal failure have two options: dialysis and transplantation. A patient may go from dialysis to transplantation. In fact, if a compatible donor (preferably a sibling) is available, a transplant is advisable. For those without a suitable donor, long-term hemodialysis is the first option.
Dialysis is defined as the diffusion of dissolved molecules through a semipermeable membrane. Several types of dialysis are available. Hemodialysis filters and cleans the blood as it passes through the semipermeable membranous tube in contact with a balanced salt solution (dialysate). Hemodialysis can be performed in a dialysis unit of a hospital or at home. It must usually be done two or three times a week, with each session lasting from three to six hours, depending on the type of membranes used and the size of the patient. Hemodialysis can lead to acute neurological changes. Lethargy, irritability, restlessness, headache, nausea, vomiting, and twitching may all occur. In some patients, neurological complications occur after dialysis is terminated. Convulsions are the most common of these consequences. In continuous abdominal peritoneal dialysis, a fresh amount of dialysate is introduced from a bag attached to a permanently implanted plastic tube. Wastes and water pass into the dialysate from the surrounding organs; then the fluid is collected four to eight hours later. Peritoneal dialysis is performed by the patient. It is continuous, so the clearance rate of wastes is higher. The most
important neurological complications of peritoneal dialysis are worsening of urea-induced brain abnormalities accompanied by twitching and, rarely, psychosis and convulsions.
Transplantation of a
kidney is considered for patients with primary renal diseases as well as end-stage renal failure resulting from any number of systemic and metabolic diseases. Success rates are highest for those suffering from lupus nephritis, gout, and cystinosis. If a kidney is received from a close relative, there is a 97 percent one-year survival rate. Even if the organ transplant comes from a nonrelative, the survival rate is still 90 percent.
Bibliography
Cameron, J. Stewart. History of the Treatment of Renal Failure by Dialysis. New York: Oxford University Press, 2002.
Catto, Graeme R. D., and David A. Power, eds. Nephrology in Clinical Practice. London: Edward Arnold, 1988.
Coffman, Thomas M., et al. Schrier's Diseases of the Kidney. 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013.
Daugirdas, John T., Peter G. Blake, and Todd S. Ing, eds. Handbook of Dialysis. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
Dische, Frederick E. Renal Pathology. 2d ed. New York: Oxford University Press, 1995.
Greenberg, Arthur, et al., eds. Primer on Kidney Diseases. 5th ed. Philadelphia: Elsevier/Saunders, 2009.
“Kidney Diseases.” MedlinePlus, March 25, 2013.
Morgan, Steven H., and Jean-Pierre Grunfeld, eds. Inherited Disorders of the Kidney: Investigation and Management. New York: Oxford University Press, 1999.
National Kidney Foundation. http://www.kidney.org.
O’Callaghan, C. A., and Barry M. Brenner. The Kidney at a Glance. Malden, Mass.: Blackwell Science, 2000.
Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow, eds. Current Medical Diagnosis and Treatment. 52d ed. New York: McGraw-Hill, 2013.
Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Kidney Failure: A Revised and Updated Directory for the Internet Age. San Diego, Calif.: ICON Health, 2005.
Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Urinary Tract Infection. San Diego, Calif.: ICON Health, 2002.