Problemas renales de la cirrosis

Abstract

Cirrhosis of the liver is a common entity frequently seen by the clinician only after initiation of edema or ascitis. Renal problems have been described for many years associated to all types of cirrhosis, and are responsible for many abnormalities of water and electrolytes seen in these patients. One of the most remarkable renal abnormalities is sodium retention, with urinary excretion (UnaV) of less than 10 mEq/1. This fact explains the common appearance of edema and ascitis even in the early states of cirrhosis. For many years two main theories have been postulated in order to explain this avid sodium retention: 1) The "underfill theory" states that the initial event is a state of peripheral vasodilatation that causes ineffective plasma volume and sodium retention by the kidney, meaning that the sodium retention is a secondary event. 2) the "overflow theory" in contrast, emphasizes that the primary event is sodium retention by the kidney, with secondary expansion of plasma volume and associated sequestration of fluid in the abdomen due to portal hypertension and a reduction of the colloid-osmotic pressure. Recent evidence is suggestive that both theories play a significant role in the avid sodium retention of cirrhosis. In order to explain the sodium retention by the kidney the following humoral factors have been postulated: increased secretion and decreased degradation of aldosterone, decreased production of prostaglandin E, increased secretion of catecholamines, decreased response to the natriuretic atrial factor and abnormalities of the kalikrein-kinin system. Although some studies have shown abnormalities in the handling of water by the kidney, most of the evidence suggest that it is due to the sodium retention. The hyponatremia seen in these patients is always secondary to excess of water and sodium and also to increased secretion of antidiuretic hormone with water retention. Although ascitis of cHrtain degree requires treatment, the presence of mild ascitis is not necessarily an indication of therapy. The first objective of treatment is weight loss through increased diuresis due to sodium restriction; only when this measure is ineffective the use of diuretics is indicated: spironolactone and furosemidH in variable dosage are the most effective agents of proven efficacy but if used inappropiately severe complications such as: Hnccfalopathy (24%), hyperazotemia (30%), hyponatremia (45%) and hypokalemia (64%) can be seen. Aside of these frequently used measures many other modalities are available such as: large volume paracentesis, peritonco-jugular shunts, ascitic fluid reinfusion, arterio-venous hemofiltration, suppressors of vasodilatation (Aramine), prosmglandin and vasopressin analogues. In advanced cirrhosis acute renal failure is often secondary to the hepatorenal syndrome, that essentially is a functional renal failure due to a severe intrarenal vasoconstriction. The kidneys of these patients function normally when transplanted experimentally and liver transplantation normalizes renal function. In terminal cirrhotics with severe complications such as hypotension, bleeding, infections, etc. acute tubular necrosis is common. The differential diagnosis can be done without difficulty through the correct evaluation of UnaV, U/P Cr, Uosm and the urinary sediment. Finally a distinct type of IgA glomerulonephritis can be seen in cirrhosis of the liver.