Renal failure, chronic
Although chronic renal failure is usually the result of a gradually progressive loss of renal function, it occasionally results from a rapidly progressive disease of sudden onset. 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.
If this condition continues unchecked, uremic toxins accumulate and produce potentially fatal physiologic changes in all major organ systems. If the patient can tolerate it, maintenance dialysis or kidney transplantation can sustain life.
Chronic renal failure may result from:
chronic glomerular disease such as glomerulonephritis
chronic infection, such as chronic pyelonephritis or tuberculosis
a congenital anomaly such as polycystic kidneys
vascular disease, such as renal nephrosclerosis or hypertension
an obstructive process such as calculi
collagen disease such as systemic lupus erythematosus
nephrotoxic drug therapy such as long-term aminoglycoside therapy
endocrine disease such as diabetic neuropathy.
Such conditions gradually destroy the nephrons and eventually cause irreversible renal failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic renal failure.
Chronic renal failure may progress through the following stages:
reduced renal reserve (glomerular filtration rate [GFR] is 40 to 70 ml/ minute)
renal insufficiency (GFR is 20 to 40 ml/ minute)
renal failure (GFR 10 to 20 ml/ minute)
end-stage renal disease (GFR is < 10 ml/minute).
Signs and symptoms
Chronic renal failure produces major changes in all body systems.
Renal and urologic changes
Initially, salt-wasting and consequent hyponatremia produce hypotension, dry mouth, loss of skin turgor, listlessness, fatigue, and nausea. Later, somnolence and confusion develop.
As the number of functioning neph-rons decreases, so does the kidneys’ capacity to excrete sodium, resulting in sodium retention and overload. Accumulation of potassium causes muscle irritability and then muscle weakness as the potassium level continues to rise.
Fluid overload and metabolic acidosis also occur. Urine output decreases; urine is very dilute and contains casts and crystals.
Renal failure leads to hypertension and arrhythmias, including life-threatening ventricular tachycardia or fibrillation. Other effects include cardiomyopathy, uremic pericarditis, pericardial effusion (and possibly cardiac tamponade), heart failure, and peripheral edema.
Pulmonary changes include reduced pulmonary macrophage activity with increased susceptibility to infection, pulmonary edema, pleuritic pain, pleural friction rub and effusions, uremic pleuritis, and uremic lung (or uremic pneumonitis). Dyspnea from heart failure also occurs, as do Kussmaul’s respirations as a result of acidosis.
Inflammation and ulceration of GI mucosa cause stomatitis, gum ulceration and bleeding and, possibly, parotitis, esophagitis, gastritis, duodenal ulcers, lesions on the small and large bowel, uremic colitis, pancreatitis, and proctitis. Other GI signs and symptoms include a metallic taste in the mouth, uremic fetor (ammonia smell to breath), anorexia, nausea, and vomiting.
Typically, the skin is pallid, yellowish bronze, dry, and scaly. Other cutaneous signs and symptoms include severe itching; purpura; ecchymoses; petechiae; uremic frost (most common in critically ill or terminal patients); thin, brittle fingernails with characteristic lines; and dry, brittle hair that may change color and fall out easily.
Restless leg syndrome, one of the first symptoms of peripheral neuropathy, causes pain, burning, and itching in the legs and feet, which may be relieved by voluntarily shaking, moving, or rocking them. Eventually, this condition progresses to paresthesia and motor nerve dysfunction (usually bilateral footdrop) unless dialysis is initiated.
Other signs and symptoms include muscle cramping and twitching, shortened memory and attention span, apathy, drowsiness, irritability, confusion, coma, and seizures. EEG changes indicate metabolic encephalopathy.
Common endocrine abnormalities include stunted growth in children (even with elevated growth hormone levels), infertility and decreased libido in both sexes, amenorrhea and cessation of menses in women, and impotence and decreased sperm production in men. Other changes include increased aldosterone secretion (related to increased renin production) and impaired carbohydrate metabolism (causing increased blood glucose levels similar to those found with diabetes mellitus).
Anemia, decreased red blood cell (RBC) survival time, blood loss from dialysis and GI bleeding, mild thrombocytopenia, and platelet defects occur. Other problems include increased bleeding and clotting disorders, demonstrated by purpura, hemorrhage from body orifices, easy bruising, ecchymoses, and petechiae.