Renal failure, chronic
Usually the end result of a gradually progressive loss of renal function, chronic renal failure also occasionally results from a rapidly progressive disease of sudden onset that gradually destroys the nephrons and eventually causes irreversible renal damage. Few symptoms develop until after more than 75% of glomerular filtration is lost; then, the remaining normal parenchyma deteriorates progressively, and symptoms worsen as renal function decreases.
Chronic renal failure may progress through these stages:
reduced renal reserve (glomerular filtration rate [GFR] 35% to 50% of normal)
renal insufficiency (GFR 20% to 35% of normal)
renal failure (GFR 20% to 25% of normal)
end-stage renal disease (GFR less than 20% of normal).
This syndrome is fatal without treatment, but maintenance dialysis or a kidney transplant can sustain life.
Causes
Chronic renal failure may result from:
chronic glomerular disease such as glomerulonephritis
chronic infections, such as chronic pyelonephritis or tuberculosis
congenital anomalies such as polycystic kidney disease
vascular diseases, such as renal nephrosclerosis or hypertension
obstructive processes such as calculi
collagen diseases such as systemic lupus erythematosus
nephrotoxic agents such as long-term aminoglycoside therapy
endocrine diseases such as diabetic neuropathy.
Complications
If chronic renal failure continues unchecked, uremic toxins accumulate and produce potentially fatal physiologic changes in all major organ systems.
Even if the patient can tolerate life-sustaining maintenance dialysis or a kidney transplant, he may still have anemia, peripheral neuropathy, cardiopulmonary and GI complications, sexual dysfunction, and skeletal defects.
Assessment
The patient’s history may include a disease or condition that can cause renal failure; however, he may not have any symptoms for a long time. Symptoms usually occur by the time the GFR is 20% to 35% of normal, and almost all body systems are affected. (See Detecting chronic renal failure, pages 792 and 793.)
Diagnostic tests
The following laboratory findings aid in the diagnosis and monitoring of chronic renal failure:
Blood studies show decreased arterial pH and bicarbonate levels, low hemoglobin and hematocrit, decreased red blood cell (RBC) survival time, mild thrombocytopenia, platelet defects, metabolic acidosis, and elevated blood urea nitrogen, serum creatinine, sodium, and potassium levels. Blood studies also show increased aldosterone secretion (related to increased renin production) and increased blood glucose levels similar to those that occur in diabetes mellitus (a sign of impaired carbohydrate metabolism). Hypertriglyceridemia and decreased high-density lipoprotein levels are common.
Arterial blood gas analysis reveals metabolic acidosis.
Urine specific gravity becomes fixed at 1.010; urinalysis may show proteinuria, glycosuria, RBCs, leukocytes, and casts and crystals, depending on the cause.
X-ray studies, including kidney-ureter-bladder radiography, excretory urography, nephrotomography, renal scan, and renal arteriography, show reduced kidney size.
Renal biopsy allows histologic identification of underlying pathology.
EEG shows changes that indicate metabolic encephalopathy.
Treatment
Conservative treatment aims to correct specific symptoms. A low-protein diet reduces the production of end products of protein metabolism that the kidneys can’t excrete. (However, a patient receiving continuous peritoneal dialysis should have a high-protein diet.) A high-calorie diet prevents ketoacidosis and the negative nitrogen balance that results in catabolism and tissue atrophy. The diet also should restrict sodium and potassium.
Maintaining fluid balance requires careful monitoring of vital signs, weight changes, and urine volume (if the patient isn’t anuric). Fluid retention can be reduced with loop diuretics such as furosemide (if some renal function remains) and with fluid restriction. Antihypertensives may be used to control blood pressure and associated edema.
Antiemetics taken before meals may relieve nausea and vomiting. Docusate can help prevent constipation.
Anemia necessitates iron and folate supplements; severe anemia requires infusion of fresh frozen packed cells or washed packed cells. Transfusions relieve anemia only temporarily. Synthetic erythropoietin (epoetin alfa) stimulates the division and differentiation of cells within the bone marrow to produce RBCs.
Drug therapy commonly relieves associated symptoms. An antipruritic such as trimeprazine or diphenhydramine can relieve itching, and calcium-containing,
phosphate-binding medications can lower serum phosphate levels. The patient also may benefit from supplementary vitamins (particularly vitamins B and D) and essential amino acids.
phosphate-binding medications can lower serum phosphate levels. The patient also may benefit from supplementary vitamins (particularly vitamins B and D) and essential amino acids.
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