scholarly journals Pathogenesis of glomerular injury in the fawn-hooded rat: early glomerular capillary hypertension predicts glomerular sclerosis.

1993 ◽  
Vol 3 (11) ◽  
pp. 1775-1782 ◽  
Author(s):  
J L Simons ◽  
A P Provoost ◽  
S Anderson ◽  
J L Troy ◽  
H G Rennke ◽  
...  

Fawn-hooded rats spontaneously develop focal and segmental glomerular sclerosis, systemic hypertension, and proteinuria at a young age. Micropuncture and morphological studies were performed in two inbred strains of fawn-hooded rats, FHH and FHL, with different susceptibilities to develop chronic renal failure. FHH rats have higher values for systolic blood pressure and proteinuria and more rapid development of focal and segmental glomerular sclerosis and subsequent chronic renal failure as compared with genetically closely related FHL rats. FHH and FHL strains and a Wistar control strain, WAG, were matched for age and were studied at 16 wk. FHH, FHL, and WAG-old (WAG-O) strains were matched for weight, and the last group was studied at 22 wk. WAG were also matched for weight to a young group of FHH rats (FHH-Y), and these were studied at 8 wk. In comparison with WAG and WAG-O rats, FHH and FHH-Y rats exhibited an increased in mean glomerular capillary hydraulic pressure (WAG, 52 +/- 1 mm Hg; WAG-O, 47 +/- 2 mm Hg; FHH, 60 +/- 2 mm Hg; FHH-Y, 65 +/- 1 mm Hg), whereas values in FHL animals were intermediate (56 +/- 2 mm Hg). No significant differences in glomerular volume were found among groups. Moderate focal and segmental glomerular sclerosis developed in FHH and FHH-Y rats, with values for older FHH rats being significantly greater than those for WAG, WAG-O, and FHL animals. Thus, the genetically determined sensitivity to develop proteinuria, focal and segmental glomerular sclerosis, and chronic renal failure in fawn-hooded rats correlated with early evidence of glomerular capillary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

1996 ◽  
Vol 7 (3) ◽  
pp. 437-442 ◽  
Author(s):  
L D Dworkin ◽  
J A Benstein ◽  
E Tolbert ◽  
H D Feiner

Salt restriction inhibits renal growth and stabilizes injury in rats with established renal disease. Male Munich-Wistar rats that underwent right nephrectomy and segmental infarction of two thirds of the left kidney were fed standard chow for 4 wk and then randomly assigned to ingest standard or low-salt chow for an additional 4 wk. Four wk after ablation, rats had systemic hypertension, proteinuria, and glomerular sclerosis. The prevalence of sclerosis, protein excretion rate, and glomerular volume increased between the fourth and eighth week in rats that were fed standard chow, however, in rats that were fed low-salt chow, the increase in glomerular volume and development of further glomerular sclerosis was prevented whereas the protein excretion rate actually declined. Micropuncture studies performed 8 wk after ablation revealed that the glomerular hydraulic pressure was elevated in remnant kidneys and was not affected by salt restriction. This study demonstrates that dietary salt restriction can prevent further glomerular injury and reduce proteinuria even when instituted in rats with established renal disease. These findings are also consistent with the hypothesis that glomerular hypertrophy promotes injury in this model of hypertension and progressive renal disease.


2020 ◽  
Vol 37 (06) ◽  
pp. 570-576
Author(s):  
Mallory Hoffman ◽  
Baha Sibai

Abstract Objective Pregnancy on dialysis is rare and few studies in this population exist. Currently, pregnancy outcomes are thought to be related to dialysis intensity. We hypothesize women requiring dialysis due to diabetes or lupus will have worse pregnancy outcomes compared with other indications for dialysis. Study Design All women receiving dialysis during pregnancy from 2012 to 2016 in a single health system were identified. Differences in perinatal outcomes among those with renal failure caused by diabetes or lupus and with other causes were evaluated. Results Sixteen women were identified, seven with diabetes or lupus causing renal failure; the remaining nine women had hypertension, focal segmental glomerular sclerosis, polycystic kidney disease, congenital hypoplastic kidneys, or neurogenic bladder. The rates of composite maternal morbidity were similar among the two groups. Composite neonatal morbidity was higher in those with renal failure caused by diabetes or lupus compared with other causes (100% vs. 29%, p = 0.028). Conclusion Despite similar dialysis intensity, the composite neonatal morbidity was higher in women with renal failure caused by diabetes or lupus compared with other etiologies. Our findings suggest that pregnancy outcome in women receiving dialysis is dependent on both the intensity of dialysis as well as the etiology of renal failure.


Nephron ◽  
1989 ◽  
Vol 51 (4) ◽  
pp. 530-535 ◽  
Author(s):  
Toru Sanai ◽  
Seiya Okuda ◽  
Kenichi Motomura ◽  
Kaoru Onoyama ◽  
Masatoshi Fujishima

1991 ◽  
Vol 1 (10) ◽  
pp. 1180-1185
Author(s):  
H M Lafferty ◽  
D L Garcia ◽  
H G Rennke ◽  
J L Troy ◽  
S Anderson ◽  
...  

To explore the role of systemic hematocrit in the vascular adaptations which characterize desoxycorticosterone-salt hypertension, studies were performed in three groups of rats with uninephrectomy, desoxycorticosterone administration, and 1% saline in the drinking water. One group received recombinant human erythropoietin to increase hematocrit, and another group was subjected to phlebotomy and fed a low-iron diet to induce anemia. Control rats exhibited systemic and glomerular capillary hypertension, proteinuria, and substantial glomerular sclerosis at 8 wk. Erythropoietin modestly increased hematocrit and blood pressure and substantially aggravated glomerular capillary pressure, proteinuria, and glomerular sclerosis. In contrast, reduction of hematocrit with a low-iron diet significantly attenuated systemic and glomerular hypertension, proteinuria, and sclerosis. It was concluded that the pace of progression of glomerular injury can be limited by chronic reduction in hematocrit, which effectively ameliorates both systemic and glomerular hypertension in this model of salt-sensitive hypertensive renal disease.


1990 ◽  
Vol 259 (2) ◽  
pp. F239-F245 ◽  
Author(s):  
P. L. Miller ◽  
H. G. Rennke ◽  
T. W. Meyer

Sprague-Dawley rats received infusions of 55-microns microspheres (groups 1 and 3) or dextrose (groups 2 and 4) into both renal arteries. Groups 1 and 2 rats were studied over 7 mo. In group 1 rats renal embolization increased the mean arterial pressure (group 1, 140 +/- 4 mmHg; group 2, 118 +/- 2 mmHg) without reducing the glomerular filtration rate (GFR; group 1, 4.69 +/- 0.16 ml/min; group 2, 4.57 +/- 0.22 ml/min). Micropuncture studies showed that systemic hypertension was accompanied by an increase in the glomerular capillary pressure of functioning nephrons in group 1 rats. Morphological studies showed that renal embolization caused both glomerular ischemia (group 1, 11.8 +/- 1.9% of glomeruli; group 2, 0.1 +/- 0.1% of glomeruli) and glomerular segmental sclerosis (group 1, 15.0 +/- 1.0% of glomeruli; group 2, 3.3 +/- 0.2% of glomeruli). Groups 3 and 4 rats were studied over 2 mo. Renal embolization again increased the mean arterial pressure without reducing the GFR in group 3 rats. Morphological studies showed that at 2 mo renal embolization caused glomerular ischemia without glomerular segmental sclerosis. These studies show that focal glomerular ischemia can cause systemic and glomerular capillary hypertension in the absence of a reduction in the GFR. They further show that focal glomerular ischemia can cause progressive sclerotic injury in the remaining, nonischemic portion of the glomerular population.


1998 ◽  
Vol 2 (1) ◽  
pp. 1-6
Author(s):  
A M El Nahas ◽  
N Tamimi

An increasing number of patients require dialysis replacement therapy every year in Europe. This reflects the large number of patients with chronic renal failure (CRF) and the progressive nature of their underlying nephropathies. Worldwide, the annual incidence of acceptance rates on renal replacement programmes varies between 25 patient per million of population (pmp) in some developing countries to 58.6 pmp in Europe, 169 pmp in the USA [I] and 194.2 pmp in Japan [2]. In Europe, there are in excess of 312 pmp on replacement therapy with France having one of the highest prevalence within the continent with 628 pmp [3]. Further, there are important differences in the incidence of end stage renal failure (ESRF) according to age, gender and race. In Western countries, the incidence of ESRF is lowest in children (10 pmp/year) and highest in the elderly (> 400 pmp/year in patients over the age of 75). The incidence of ESRF is higher in males. In the United States, the incidence of ESRF is higher in Afro-Carribeans and native Americans [4]. This reflects both an increased prevalence of CRF in these ethnic minorities as well as a higher rate of progression [4]. It also reflects the higher incidence of systemic hypertension and diabetic nephropathy in black and native Americans respectively [4].In the United Kingdom, the incidence of ESRF is higher in Asians [5].


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