E. Valvo

Hypertension of Polycystic Kidney Disease: Mechanisms and Hemodynamic Alterations

32 polycystic kidney disease (PKD) patients, 16 with normal 16 with variably decreased renal function, were studied; 12 were normotensive, 20 were hypertensive. Mean arterial pressure (MAP) was 90 +/- 8 mm Hg in the normotensive group and 117 +/- 17 in hypertensive patients; plasma renin activity (PRA) was similar. The glomerular filtration rate (GFR) was lower, but not significantly, in the hypertensive group and plasma volume (PV) was higher in hypertensive patients (normotensive 40.25 +/- 3.47 ml/kg body weight; hypertensive 46.30 +/- 3.54). No correlation was found between MAP, and PRA or GFR but MAP correlated with PV. Cardiac output was higher in hypertensive patients (normotensive 3.48 +/- 0.70 l/min/m2; hypertensive 3.89 +/- 1.47), also total peripheral resistance was higher in the hypertensive group (normotensive 2,035 +/- 503 dyn/s/cm-5/m2; hypertensive 2,577 +/- 808). Cardiac output and PV showed a high degree of correlation, but no correlation was seen between total peripheral resistance and PV, or PRA. The hypertensive patients were divided into two groups: one with hypertension of less than 2 years duration and one with more than 2 years but with similar GFR, PRA, PV and hemodynamic pattern. Our data indicate that hypertension in PKD is volume-dependent; that the increase in PV was not related to the loss of GFR, and that the role of the renin-angiotensin system in maintaining the hypertensive state is not well defined. Hemodynamically hypertension is characterized by high cardiac output and total peripheral resistance independent of the duration of hypertension.

Hypertension in primary immunoglobulin A nephropathy (Berger's disease): hemodynamic alterations and mechanisms

Twenty-two patients with primary IgA nephropathy (Bergers disease), 12 with normal and 10 with high blood pressure, were studied. The mean intra-arterial pressure was 88 +/- 6 mm Hg in the normotensive group and 113 +/- 10mm Hg in hypertensive patients; plasma renin activity was high in normotensives and normal in hypertensives. The glomerular filtration rate was 83 +/- 23 and 73 +/- 26 ml/m in 1.73 m2 in normotensive and hypertensive patients, respectively (p = n.s.). Blood volume was high in IgA nephropathy patients: 82 +/- 12 ml/kg body weight in normotensives and 96 +/- 7 ml/kg body weight in hypertensives. Mean arterial pressure was significantly correlated with blood volume (r = 0.541, p less than 0.01), but not with plasma renin activity and glomerular filtration rate. The cardiac index was high in both groups: 4.20 +/- 0.88 liters/min/m2 in normotensive and 3.95 +/- 0.87 liters/min/m2 in hypertensive patients. The total peripheral resistance index was significantly lower than normal in normotensives (1,659 +/- 387 dyn/s/cm-5/m2) and significantly higher (2,419 +/- 562 dyn/s/cm-5 m2) in hypertensives. The cardiac index did not correlate with blood volume and mean arterial pressure; a positive correlation was found between mean arterial pressure and peripheral vascular resistance (r = 0.630, p less than 0.01). No correlation was observed between blood volume and plasma renin activity. Our study indicates that hypertension in IgA nephropathy is primarily volume dependent, and that this increase in blood volume is not related to the deterioration of renal function. The role of the renin-angiotensin system in the maintenance of the hypertension is not well-defined.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbohydrate metabolism in patients with nephrotic syndrome and normal renal function

The effects of a standard oral glucose tolerance test (OGTT) on the serum concentrations of glucose, insulin, growth hormone (GH) and cortisol were evaluated in 38 adult patients with primary nephrotic syndrome and with normal renal function, and in 10 normal subjects. 14 patients had a diabetic-like response and 24 were not different from controls. In both groups of patients an increase in insulin pool secretion, probably due to elevated serum GH levels, was observed. The increased GH values were not related to serum albumin nor to urinary protein losses. No significant difference in serum cortisol values was observed in patients with nephrotic syndrome as compared to controls. There was no strict correlation between the various histologic lesions and the metabolic abnormalities. However, patients with a diabetic-like response to OGTT had a higher frequency of membranous glomerulopathy or focal glomerular sclerosis.

Clinical Significance of Urinary Fibrinogen Degradation Products in Renal Disease

The investigation of fibrinogen degradation products (FDP) in urine has been suggested as a reliable method to detect the glomerular deposition of fibrin. Urinary FDP were investigated in 246 patients with renal disease by means of a latex test in 100 of them (positive in 54%); in the remaining 146 patients the Merskey method was used which gave positive results in 26% of them. A significant correlation between urinary protein excretion and FDP was only observed in those patients examined with the latex test. In patients investigated with the Merskey method, the simultaneous determination of serum FDP showed no correlation between FDP values in serum and urine. In those patients studied by means of renal biopsy, a poor correlation was observed between immunofluorescence and electron microscopic evidence of fibrin deposition and urinary FDP. In conclusion, isolated urinary FDP detection is not an index of pathologic coagulation in the glomeruli.