Our results indicate that renal failure is greatly underestimated on the basis of serum creatinine level and Ccr in cirrhotic patients. Clinical implications of this observation include excessive dosage of potentially nephrotoxic drugs and failure to recognize renal impairment induced by such medical treatments as diuretic therapy or paracentesis.

Summary:The plasma level of carnitine, a co-factor involved in many metabolic reactions, is high in alcoholic liver cirrhosis, due to an increased amount of esterified carnitine. To determine if this alteration is linked to alcoholic liver disease or to liver cirrhosis per se, total carnitine, free carnitine, total esterified carnitine, short chain acylcarnitine and long chain acylcarnitine were measured in 41 patients suffering from liver cirrhosis of different aetiology and severity. In 19 of these patients, acetylcarnitine was also measured. Moreover, multivariate analysis was performed to assess the association of carnitine plasma levels with nutritional and liver disease indices.Of the nutritional indices (creatinine/height ratio, mid upper arm muscle circumference and triceps skinfold) only triceps skinfold appeared to be weakly correlated with carnitine (with long chain acylcarnitine).Significantly high levels of acetylcarnitine, short chain acylcarnitine, total esterified carnitine and total carnitine were found in cirrhotics independently of the aetiology of cirrhosis, even though a trend towards higher levels of acetylcarnitine was evident in heavy drinkers.Direct correlations of -glutamyltransferase with acetylcarnitine, acetylcarnitine/free carnitine, short chain acylcarnitine/free carnitine and total esterified carnitine/free carnitine were found. Carnitine plasma levels did not differ in the three Pugh-Chiltfs classes; however, a trend towards higher levels of acetylcarnitine was found in Pugh-ChilcTs class C.

Renal tubular sodium handling was evaluated in 27 non-azotemic cirrhotic patients with ascites and positive sodium balance and in 17 controls after at least 5 days of a constant sodium intake using the lithium clearance as an index of fluid delivery to the distal tubule. Plasma renin activity and plasma aldosterone were also evaluated. Sodium fractional excretion, filtered sodium load, absolute sodium distal delivery, lithium fractional excretion and absolute distal sodium reabsorption were significantly lower in cirrhotics than in controls (0.58 +/- 0.11 vs. 1.29 +/- 0.12%, P less than 0.001; 12529 +/- 677 vs. 15707 +/- 796 microEq min-1 1.73 m-2 BSA, P less than 0.005; 2384 +/- 135.2 vs. 3685 +/- 219.3 microEq min-1 1.73 m-2 BSA, P less than 0.001; 19.5 +/- 1.0 vs. 24.2 +/- 1.3%, P less than 0.01; 2299 +/- 127 vs. 3485 +/- 214 microEq min-1 1.73 m-2 BSA, P less than 0.001, respectively). A correlation was found between lithium clearance and sodium clearance only in cirrhotic patients (r = 0.62; P less than 0.01). Distal sodium reabsorption evaluated as a per cent of filtered sodium load was lower in cirrhotics than in controls (19.1 +/- 1.0 vs. 22.4 +/- 1.2%, P less than 0.05) while distal sodium reabsorption evaluated as a per cent of sodium distal delivery was higher in cirrhotics than in controls (96.7 +/- 0.4 vs. 94.4 +/- 0.5%, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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A juxtaglomerular cell tumor (JGCT) was found in a 40 year old woman. For 5 years she had mild hypertension, responding to classical anti-hypertensive treatment, then she became severely hypertensive. Two renal angiographies and a CT scan were reported as normal. A second CT scan and third selective renal angiography were diagnostic, associated with lateralization of renin in renal vein measurement. Light, electron microscopy and immunohistochemistry of the resected tumor confirmed the diagnosis of renin-secreting juxtaglomerular cell tumor of the kidney.