Can systemic lupus erythematosus be the cause of collapsing glomerulopathy?

Collapsing glomerulopathy is a severe form of glomerular injury, closely associated with HIV infection, characterized by the collapsing feature of glomerular damage with frequent tubulointerstitial involvement and rapid progression to terminal renal failure. The etiopathogenesis in non-HIV infected patients remains obscure. We reported a patient whose diagnosis of collapsing glomerulopathy (CG) and systemic lupus erythematosus (SLE) was done simultaneously and described the diseases characteristics suggesting that SLE could be an etiologic factor for the induction of this glomerulopathy, clinical evolution and treatment.

AIDS-associated renal tuberculosis.

In order to study the prevalence and the clinical features of renal tuberculosis associated with AIDS, we studied the renal tissue of the necropsies made in 46 AIDS patients under light microscopy. We found renal tuberculous granuloma in 11 (23%) patients (in 3 without previous diagnosis of renal or extrarenal tuberculosis) and only 4 of them presented moderate hematuria or pyuria sterile. As subclinical renal tuberculosis was frequent in this group of AIDS patients, the urine culture for Mycobacterium tuberculosis may be useful for diagnosing tuberculosis in AIDS patients.

Renal response to angiotensin after short-term angiotensin converting enzyme inhibition.

In 13 normotensive subjects on a normal sodium diet, we studied hormonal, blood pressure, and renal vascular changes and dextran sieving profiles induced by infusion of exogenous angiotensin II (Ang II) (5 ng.kg-1.min-1). during baseline conditions and after 5 days of administration of the angiotensin converting enzyme inhibitor cilazapril. Cilazapril induced a renal vasodilative effect without affecting supine blood pressure and glomerular filtration rate. Fractional dextran clearances were significantly decreased for dextran of effective radius ranging from 3.0 to 4.0 nm. This shift was primarily related to an increase in glomerular capillary plasma flow, because no change was observed in the transcapillary glomerular pressure gradient, the ultrafiltration coefficient, or the membrane parameters. Ang II elicited a slight pressor response accompanied by hormonal, antinatriuretic, and renal hemodynamic changes that were similar during and before short-term angiotensin converting enzyme inhibition. Dextran sieving curves were unchanged by a low dose of Ang II. However, the transcapillary glomerular pressure gradient and the ultrafiltration coefficient were computed to increase by 19.4% and to decrease by 44.2%, respectively, whereas membrane parameters were unaffected. When superimposed onto short-term angiotensin converting enzyme inhibition, glomerular response to this unique dose of Ang II was similar to that induced by Ang II alone. These findings indirectly suggest that most, if not all, of the renal effects of cilazapril are mediated through suppression of Ang II formation.

Predisposition to essential hypertension and renal hemodynamics in recent-onset insulin-dependent diabetic patients.

The offspring of essential hypertensive parents have been found to exhibit abnormalities in renal hemodynamics and sodium handling before the eventual occurrence of hypertension. The reported abnormalities represent a wide spectrum of changes including increased GFR, normal or decreased RPF, slight increase in blood pressure (although within the normal range), and an exaggerated natriuresis response to a sodium load. The heterogeneity of these abnormalities may reflect the specific conditions of the studies, the lability of the changes, or different subgroups of subjects with genetic predisposition to essential hypertension. Several lines of evidence have suggested a relationship between hypertension and the development of diabetic nephropathy in insulin-dependent diabetics. This laboratory has found that recent-onset insulin-dependent diabetics can exhibit renal hemodynamics abnormalities very early in the course of diabetes according to a positive or negative family history of essential hypertension. These changes include increased GFR and mean arterial pressure, but no differences in renal sodium and lithium handling in diabetics with a genetic predisposition to essential hypertension. In addition, diabetics with a positive family history of essential hypertension exhibited a more-marked vasodilative response to an acute interruption of the renin-angiotensin system, further suggesting inadequate angiotensin modulation of renal vascular tone. The significance of these abnormalities in relation to the development of diabetic nephropathy requires further investigation.

Renal abnormalities in normotensive insulin-dependent diabetic offspring of hypertensive parents.

To assess the effects of genetic predisposition of essential hypertension on early renal function in recent insulin-dependent diabetics, we studied inulin, para-aminohippuric, sodium, and lithium clearances in 69 unselected diabetics with (n = 20) and without (n = 49) a family history of essential hypertension. Despite similar metabolic control, glomerular filtration rate and mean arterial pressure were significantly higher in diabetics with than in those without a family history of hypertension. However, no difference was found between the two groups regarding renal vascular resistance, sodium excretion, or fractional proximal and distal sodium reabsorption. Renal responses to acute captopril (75 mg) administration were evaluated in 27 patients (six with family history of hypertension). Captopril decreased filtration fraction and mean arterial pressure similarly in both groups, whereas glomerular filtration rate and renal vascular resistance decreased more dramatically in diabetics with family history of hypertension. These findings indirectly suggest an abnormal response to angiotensin of vascular tone in recent diabetics with familial predisposition to hypertension. Renal response to acute nicardipine (2.5 mg i.v.) administration was analyzed in 24 patients (five with family history of hypertension). In both groups, nicardipine similarly decreased mean arterial pressure and renal vascular resistance and induced a marked natriuretic effect due to a predominant reduction in proximal reabsorption of sodium. However, the increase in sodium excretion was twofold to threefold more pronounced in diabetics with a family history of hypertension. Whether these early renal abnormalities may contribute to the risk of diabetic nephropathy, as suggested by retrospective studies, remains to be determined.

Glomerular disease and human immunodeficiency virus infection in Brazil.

Clinically overt glomerular disease was detected in 6 (1.1%) of 543 patients with HIV infection followed at a Brazilian National Referral Center for AIDS. In 4 cases, glomerulosclerosis was present (focal and segmental in 3, diffuse and global in 1) and rapid progression to terminal renal failure was observed 1-10 months after clinical presentation. The other 2 patients died with normal renal function, and autopsy studies suggested the diagnosis of minimal change disease. Clinically overt glomerular disease was significantly more common among Black patients, whether all the cases with glomerulopathy (p < 0.001) or just the cases with glomerular sclerosis were considered (p = 0.011). Autopsy study of renal fragments from patients without clinical evidence of glomerular disease was additionally performed and revealed the presence of focal and segmental glomerulosclerosis in 3 cases (7.5%). We concluded that a glomerulopathy with clinicopathological features which match the definition of HIV nephropathy can be found among Brazilian patients with HIV infection. Accordingly to what has been described in American series, Brazilian Black patients seem to be at increased risk of the development of that nephropathy.

Renal effects of angiotensin II in normotensive subjects on short-term cilazapril treatment.

In 13 normotensive subjects on a normal sodium diet, we studied renal vascular, blood pressure, and hormonal changes induced by infusion of exogenous angiotensin II (Ang II) (5 ng/kg/min) during baseline conditions and after 5 days of cilazapril administration. In both conditions, Ang II elicited a slight pressor response accompanied by renal hemodynamic and hormonal changes that were similar. This suggests that hourly changes in Ang II concentrations and/or in Ang II receptor density after short-term administration of the angiotensin-converting enzyme (ACE) inhibitor cilazapril does not significantly affect renal vascular reactivity. In addition, these results also indirectly suggest that most of the renal effects of ACE inhibition are mediated through suppression of Ang II formation.

[Hypertension induced by cyclosporin A in insulin-dependent diabetic patients. A one-year follow-up]. / Hypertension induite par la ciclosporine A chez les sujets diabétiques insulinodépendants. Suivi à un an.

UNLABELLED: Forty-five recent insulin-dependent diabetics (IDD) were treated with cyclosporine A (CsA) 7.5 mg/kg b.i.d. as single immunosuppressive therapy to achieve remission of diabetes. Measurements of mean arterial pressure (MAP), glomerular filtration rate (GFR:inulin clearance), renal vascular resistance (RVR: MAP x [1-haematocrit] divided by PAH clearance), absolute (UNa.V) and fractional (FENa) urinary sodium excretion, were performed initially (M0) and after 3 (M3) and 12 (M12) months of treatment. Results were (mean +/- SD): [table: see text] Prevalence of hypertension defined as MAP greater than or equal to 107 mmHg was 12% at M3 and 24% at M12. Whereas the maximal changes in GFR and RVR occurred at M3, MAP increased further and sodium excretion decreased at M12. IN CONCLUSION: 1) CyA-induced increase in blood pressure paralleled that in RVR at M3 and decreased sodium excretion at M12. 2) There was a dissociation between MAP and GFR changes after 12 months of treatment with CyA.