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V Woronik

Publications and source records attributed to V Woronik.

6 recordsLinked to original sources
PubMed2007

Decreased in vitro osteoblast proliferation and low turnover bone disease in nonuremic proteinuric patients.

Patients with proteinuria, even those with normal glomerular filtration rate, often present abnormal bone histology. We evaluated bone histology and the in vitro proliferation of osteoblasts in samples obtained from 17 proteinuric patients with primary glomerulopathies. Histomorphometric analysis of bone biopsies was performed, and bone fragments were obtained for osteoblast culture, in which we evaluated cell proliferation. In comparison to controls, patients presented lower trabecular bone volume (20.9+/-14.5% vs 26.8+/-5.9%; P=0.0008); lower trabecular number (1.7+/-0.2/mm vs 2.0+/-0.3/mm; P=0.004); and greater trabecular separation (475.5+/-96.4 microm vs 368.3+/-86.2 microm, P=0.0002). We also found alterations in bone formation and resorption: lower osteoid volume (0.9+/-0.7% vs 2.0+/-1.4%; P=0.0022); lower osteoid thickness (6.4+/-2.8 microm vs 11.5+/-3.2 microm; P<0.0001); less mineralizing surface (4.6+/-3.1% vs 13.5+/-6.0%; P<0.0001); lower bone formation rate (0.03+/-0.04 microm(3)/microm(2)/day vs 0.09+/-0.05 microm(3)/microm(2)/day; P<0.0001); and greater osteoclast surface (0.35+/-0.6 vs 0.05+/-0.1%, P=0.0016). Mean in vitro osteoblast proliferation was lower in patients than in controls (910.2+/-437.1 vs 2261.0+/-1121.0 d.p.m./well, P=0.0016). Serum concentrations of 25-hydroxyvitamin-D(3) correlated negatively with proteinuria and positively with in vitro osteoblast proliferation. Our results demonstrate that nonuremic proteinuric glomerulonephritic patients present bone structure disorder, low bone formation and high bone resorption, as well as low osteoblast proliferation.

Adult↗
PubMed2004

Comparative study of IgA nephropathy with and without crescents.

Glomerular crescents were analyzed as a prognostic factor in retrospectively reviewed data from 144 patients with biopsy-proven IgA nephropathy. Crescents were found in 26 (18%) patients, and detected in 2 to 100% of glomeruli in each specimen. In 5% of the patients more than 50% of the glomeruli were affected. Thirty patients with IgA nephropathy without crescents were studied as a control group. Mean age was 30.3 +/- 9.4 and 30.2 +/- 12.0 years for the patients with and without crescents, respectively, and males prevailed in both groups. The length of follow-up was 23.2 +/- 41.6 months for patients with crescents and 29.3 +/- 35.3 months for patients without crescents. Eighty percent of the patients with crescents were hypertensive, compared to 27% of the non-crescent control group (P < 0.05). Mean serum creatinine at the time of diagnosis was 3.9 +/- 2.9 and 1.9 +/- 2.1 mg/dl for the patients with and without crescents, respectively. Initial urinary protein excretion was higher in patients with crescents (4.6 +/- 3.5 vs 1.2 +/- 0.9 g/day; P < 0.05). At the end of follow-up 17 patients (77.3%) from the crescent group and 3 (11.1%) from the non-crescent group had end-stage renal disease (P < 0.0001). The presence of crescents was associated with higher levels of initial serum creatinine and urinary protein excretion, and a higher frequency of hypertension and progression to end-stage renal disease.

Biomarkers↗
PubMed1998

Glycosuria in glomerular diseases: histopathology and clinical correlations.

There are doubts about the presence of glycosuria and the progress of glomerular disease. Some reports suggest that glycosuria could be an index of a more severe tubulointerstitial lesion. We investigated the presence of glycosuria in 60 patients with primary glomerular diseases: 17 patients (28%) had glycosuria and 43 patients (72%) were glycosuria free. The two groups were similar in age, arterial pressure and sex. Serum creatinine was higher in patients with glycosuria (2.0 +/- 1.7 vs 1.3 +/- 0.9 mg/dl, P < 0.05). The protein excretion rate was 7.5 +/- 3.7 vs 5.3 +/- 4.2 g/day (P > 0.05) in patients with and without glycosuria, respectively, while serum albumin was lower in patients with glycosuria (1.7 +/- 0.6 vs 2.7 +/- 1.0 g/dl, P < 0.05). Several histological forms were present in the group with glycosuria, with membraneous glomerulonephritis being the most frequent. Histological evidence of tubular atrophy and interstitial fibrosis prevailed in patients with glycosuria, suggesting a poor prognosis for these patients. We may conclude that the presence of glycosuria in patients with glomerular disease is associated with more pronounced tubular atrophy and interstitial fibrosis and therefore imply a poorer prognosis.

Adult↗
PubMed1993

Snakebite-induced acute renal failure: an experimental model.

Acute renal failure (ARF) has been frequently reported after bites from the Viperidae snake family. The lack of a reproducible animal model has hampered the study of renal damage mechanisms. Intravenous injection of rats with 0.4 mg/kg of Bothrops jararaca venom produced functional and morphologic changes similar to those observed in human snakebite-induced ARF. There was an acute and significant decrease in the glomerular filtration rate, diuresis, and renal plasma flow. Serum fibrinogen levels decreased significantly. There was intravascular hemolysis, as shown by a significant decrease in hematocrit, and an increase in plasma lactate dehydrogenase levels and free hemoglobin. Blood pressure and serum creatine phosphokinase levels were not affected. Light and electron microscopy showed massive fibrin deposition in glomerular capillaries, proximal and distal tubular necrosis, and hemolyzed red blood cell casts in renal tubules. Based on these findings, a model of snakebite-induced ARF was achieved. Ischemia related to glomerular coagulation and intravascular hemolysis were the most important pathogenic factors causing a decrease in the glomerular filtration rate, although a direct venom nephrotoxicity cannot be excluded.

Acute Kidney Injury↗
PubMed1991

Bicarbonate reabsorption and electrophysiology of proximal tubules in uninephrectomized rats.

1. The kinetics of acidification of luminal fluid in hypertrophied proximal tubules after unilateral nephrectomy was studied by stationary microperfusion and continuous measurement of luminal pH with antimony microelectrodes. 2. Trans-epithelial and basolateral membrane electrical potential differences were measured in order to detect modifications in electrogenic transport mechanisms under these conditions. 3. The values of stationary pH and HCO3- concentration were significantly lower, the mean acidification half-time was not different and net reabsorptive HCO3- fluxes in proximal tubules were significantly increased in uninephrectomized rats. According to an electrical analogue model, these results suggest (a) a reduction in the internal series resistance of the H+ pump, caused perhaps by an increased density of pump sites, and (b) an increase in the protonmotive force of the pump. 4. The trans-epithelial electrical potential difference measured in free flow conditions was significantly more lumen-positive in uninephrectomized rats. The trans-epithelial electrical potential difference measured during intraluminal perfusion with Ringer solution containing 30 mmol/l HCO3- was significantly more negative in all groups studied. In uninephrectomized rats treated with acetazolamide, the trans-epithelial electrical potential difference was more lumen-negative than that in untreated uninephrectomized rats. These results are compatible with a steeper transepithelial Cl- gradient as well as with electrogenic, active H+ secretion. 5. There was no significant difference in the basolateral electrical potential difference between control and uninephrectomized rats. 6. In conclusion, our data show an increase in the transport rates of HCO3- in the proximal tubule of uninephrectomized rats, which may be due to an increase in the density of transporters in the brush-border membrane, and an increased ability of the transport mechanism to create H+ gradients.

Absorption↗