We report the clinical outcome of 105 essential mixed cryoglobulinemia (EMC) patients with renal involvement collected throughout 25 years in three renal Units of Milan. The median follow-up was 72 months since renal biopsy and 131 months since the clinical onset of EMC. Patient survival was 49% at 10 years after renal biopsy. Forty-two patients died primarily from cardiovascular and liver disease or infection, whereas 15 patients developed chronic renal failure. Two patients had a complete remission of the disease while 15 had a remission only of renal signs. Thirty-one patients are alive with persistent renal and extrarenal manifestations. Anti-HCV antibodies were retrospectively detected in 34 patients and were present in 85% of them. This variable was not included in the statistical evaluation. At multivariate analysis, age older than 50 years, purpura, splenomegaly, cryocrit levels higher than 10%, C3 plasma levels lower than 54 mg/dl, and serum creatinine higher than 1.5 mg/dl were independent risk factors for death or dialysis. In conclusion, several factors may influence the outcome of patients with EMC nephritis. Markers of disease activity and an impaired renal function can herald a bad prognosis. It should be stressed, however, that only a minority of patients eventually develop renal failure, probably because in the most severe cases patients die earlier.
Cardiac arrhythmias are a frequent event in chronic haemodialysis patients, and their pathogenesis is still poorly understood. We evaluated plasma K+ (PK), intraerythrocytic K+ (EK) and acid-base changes during haemodialysis in six patients with frequent arrhythmias (A-pts), and in six (used as controls) nonarrhythmic dialysis patients (C-pts). PK decreased significantly (P less than 0.01) during haemodialysis in both groups: A-pts (pre HD: 4.81 +/- 0.52 mM; 1st hour: 3.66 +/- 0.44; end HD: 3.17 +/- 0.38) and C-pts (4.75 +/- 0.80; 3.71 +/- 0.32 and 3.18 +/- 0.18 respectively) without any significant difference at any time between the two groups. Predialysis arterial pH and HCO3 were similar in A-pts (7.33 +/- 0.07 and 22.1 +/- 4.5 mM) and C-pts (7.29 +/- 0.04 and 19.7 +/- 2.6 mM) but an apparently better correction of acidosis within the treatment was seen in A-pts (arterial pH 1st hour: 7.38 +/- 0.07; end HD: 7.39 +/- 0.07) than C-pts (1st hour: 7.31 +/- 0.02, P less than 0.05 versus A-pts; end HD: 7.33 +/- 0.03, P less than 0.05 versus A-pts). EK was significantly (P less than 0.01) greater at all times in C-pts (pre HD: 90.6 +/- 15.7 mmol/l RBC; 1st hour: 93.3 +/- 11.7; end HD 96.6 +/- 10.7) than A-pts (72.1 +/- 9.0; 77.2 +/- 3.7 and 79.3 +/- 8.4, respectively). We conclude that haemodialysis patients with arrhythmias have a decreased intraerythrocytic K content in comparison with other patients despite similar PK values; this finding might constitute a predisposing factor for arrhythmias.
Six adult patients (4 females and 2 males, age range 26-57 years) with Gitelman’s syndrome (GS) were treated with spironolactone 200-300 mg/day (n = 5) and/or amiloride 10-30 mg/day (n = 3) for 1-18 months. The patients had hypokalemia, hyperreninemia, chloride-resistant metabolic alkalosis, renal hypomagnesemia (n = 5), and hypocalciuria (n = 5). Free water clearance studies during maximal water diuresis and furosemide administration were suggestive of a solute reabsorptive defect beyond the loop of Henle. Antialdosterone therapy induced a significant increase of Pk (from 2.6 ± 0.4 to 3.4 ± 0.4 τaM\ p < 0.0001) and a decrease of Cĸ (from 21.4 ± 13.2 to 10.6 ± 4.8 ml/ min, p < 0.02) and FEK (from 21.0 ± 13.6 to 13.4 ± 5.7%; p < 0.03); PMg increased from 1.38 ± 0.38 to 1.64 ± 0.21 mg/dl (p < 0.03) with a parallel fall of CMg (from 5.5 ± 2.3 to 2.9 ± 1.5 ml/min; p < 0.02) and FEMg (from 5.7 ± 2.6 to 2.9 ± 0.6%; p < 0.05); arterial blood pH and HCO-3 did not change (P = plasma, C = clearance, FE = fractional excretion). The creatinine clearance fell (from 90.5 ± 16.8 to 65.8 ± 20.9 ml/min; p < 0.05), and Prenin rose (from 16.6 ± 8.9 to 35.3 ± 25.3 ng/ml/h;p < 0.02, as did Paldo (from 26.1 ± 12.3 to 109 ± 82.6ng/dl; p < 0.01), indicating extracellular fluid volume contraction; however no significant clinical symptoms of hypovolemia ensued. Despite increased Paldo levels, estimated transtubular K gradient in K secretory sites fell (from 8.0 ± 4.0 to 6.7 ± 3.4; p < 0.01), confirming blunted aldosterone tubular effect. At the dosages employed, spironolactone induced a greater increase of Pĸ (0.81 ± 0.52 mM) than amiloride (0.07 ± 0.41; p < 0.001). In conclusion, antialdosterone therapy is effective in ameliorating hypokalemia and hypomagnesemia in GS. Its effects appear to result mainly from a direct tubular effect on K secretion and Mg reabsorption; extracellular fluid volume contraction appears also to occur during therapy, but has no relevant clinical effects. These results confirm that hypokalemia in GS is more a consequence of increased tubular secretion in the cortical collecting tubule than of impaired tubular K reabsorption; moreover, impaired tubular Mg conservation in GS might also occur in more distal segments of the nephron than previously supposed.
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