Transient defects in renal tubular function are common in patients with chronic alcoholism and may contribute to their abnormalities of serum electrolyte and blood acid-base profiles.

Erythropoietin therapy lowers plasma histamine concentrations in patients with uremia and can result in marked improvement of pruritus.

The response of intraocular pressure (IOP) to hemodialysis was investigated in 55 patients with end-stage kidney disease enrolled in a chronic dialysis program. The mean level of IOP, measured by the Goldman applanation tonometer, before dialysis was slightly lower than that of a control group of 50 healthy subjects (14.9 +/- 2 mm Hg vs 15.6 +/- 1.9 mm Hg. p = .07). During dialysis IOP underwent an excessive rise (7.8 to 12.5 mm Hg) in 10 patients (group 1), remained unchanged (variations below 2 mm Hg) in 41 patients (group 2), and decreased (3.1 to 5.1 mm Hg) in 4 patients (group 3). In group 1 patients, gonioscopy showed a narrow angle between iris and lateral cornea. Conversely, the anterior chamber angle was normal in patients of groups 2 and 3. The effect of a 7-day course of acetazolamide therapy (500 mg per day orally) on IOP was investigated in group 1 patients. Acetazolamide was capable of preventing the excessive IOP rise during dialysis. The mean reduction of such a dialytic rise was 8.1 mm Hg. However, despite this effect, in these patients the IOP level after dialysis still remained significantly higher than that of patients of group 2 (18.1 +/- 1 mm Hg vs 14.9 +/- 0.8 mm Hg. p less than .0001). Acetazolamide therapy precipitated in all patients a severe metabolic acidosis (blood pH fell from 7.38 +/- 0.02 to 7.24 +/- 0.03, p less than .0001; and bicarbonate concentration from 21 +/- 2.5 mmol/liter to 12.3 +/- 2.4 mmol/liter, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

Recent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid-base disturbances commonly observed in these patients, and possibly in alcohol-induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti-inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol-induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.