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N Schor

Publications and source records attributed to N Schor.

At least 37 records · Page 2Linked to original sources
PubMed2000

Mechanisms involved in calcium oxalate endocytosis by Madin-Darby canine kidney cells.

Calcium oxalate (CaOx) crystals adhere to and are internalized by tubular renal cells and it seems that this interaction is related (positively or negatively) to the appearance of urinary calculi. The present study analyzes a series of mechanisms possibly involved in CaOx uptake by Madin-Darby canine kidney (MDCK) cells. CaOx crystals were added to MDCK cell cultures and endocytosis was evaluated by polarized light microscopy. This process was inhibited by an increase in intracellular calcium by means of ionomycin (100 nM; N = 6; 43.9% inhibition; P<0.001) or thapsigargin (1 microM; N = 6; 33. 3% inhibition; P<0.005) administration, and via blockade of cytoskeleton assembly by the addition of colchicine (10 microM; N = 8; 46.1% inhibition; P<0.001) or cytochalasin B (10 microM; N = 8; 34.2% inhibition; P<0.001). Furthermore, CaOx uptake was reduced when the activity of protein kinase C was inhibited by staurosporine (10 nM; N = 6; 44% inhibition; P<0.01), or that of cyclo-oxygenase by indomethacin (3 microM; N = 12; 17.2% inhibition; P<0.05); however, the uptake was unaffected by modulation of potassium channel activity with glibenclamide (3 microM; N = 6), tetraethylammonium (1 mM; N = 6) or cromakalim (1 microM; N = 6). Taken together, these data indicate that the process of CaOx internalization by renal tubular cells is similar to the endocytosis reported for other systems. These findings may be relevant to cellular phenomena involved in early stages of the formation of renal stones.

Animals↗
PubMed2000

High sodium chloride intake is associated with low bone density in calcium stone-forming patients.

BACKGROUND: Although renal stone disease has been associated with reduced bone mass, the impact of nutrient intake on bone loss is unknown. SUBJECTS AND METHODS: The present study was undertaken to investigate the influence of nutrient intake on bone density of 85 calcium stone-forming (CSF) patients (47 male and 38 premenopausal females) aged 41+/-11 years (X+/-SD). Bone mineral density (BMD) was measured using dual energy X-ray absorptiometry at the lumbar spine (L2-L4) and femoral neck sites, and low BMD was defined as a T score < -1 (WHO criteria). A 4-day dietary record and a 24-hour urine sample were obtained from each patient for the assessment of nutrient intake and urinary calcium (U(Ca)), sodium (U(Na)), phosphate and creatinine excretion. RESULTS: Forty-eight patients (56%) presented normal BMD and 37 (44%) low BMD. There were no statistical differences regarding age, weight, height, body mass index, protein, calcium and phosphorus intakes between both groups. The mean U(Ca), phosphorus and nitrogen appearance also did not differ between groups. However, there was a higher percentage of hypercalciuria among low vs normal BMD patients (62 vs 33%, p < 0.05). Low BMD patients presented a higher mean sodium chloride (NaCl) intake and excretion (UNa) than normal BMD (14+/-5 vs 12+/-4 g/day and 246+/-85 vs 204+/-68 mEq/day, respectively p < 0.05). The percentage of patients presenting NaCl intake > or = 16 g/day was also higher among low vs normal BMD patients (35 vs 12%, p < 0.05). After adjustment for calcium and protein intakes, age, weight, body mass index, urinary calcium, citrate and uric acid excretion, and duration of stone disease, multiple-regression analysis showed that a high NaCl intake (> or = 16 g/day) was the single variable that was predictive of risk of low bone density in CSF patients (odds ratio = 3.8). CONCLUSION: These data suggest that reducing salt intake should be recommended for CSF patients presenting hypercalciuria and osteopenia.

Absorptiometry, Photon↗
PubMed1999

Effects of kinins upon cytosolic calcium concentrations in mouse mesangial cells.

Bradykinin (BK) induces increases in cytosolic calcium concentration [Ca++]i in several cell lines. Because the role of BK in the renal system, particularly in mesangial cell (MC), is not clear, we investigated the effects of kinins on [Ca++]i in mouse-immortalized MC. [Ca++]i was evaluated by spectrofluorometry and expressed as a ratio between the obtained and basal [Ca++]i. BK (0.1 microM) induced a non-sustained increase in [Ca++]i (4.70 +/- 0.27; N = 28). A similar effect was observed with the B2 receptor agonist, Tyr8-BK (0.1 microM, 3.34 +/- 0.48; N = 7), while B1 receptor agonists, des-Arg10-Kallidin (Kal) (1 microM, N = 11) and des-Arg9-BK (1 microM, N = 8), exhibited only discrete responses (1.45 +/- 0.08 and 1.12 +/- 0.04, respectively). Cross-desensitization was seen between BK and Tyr8-BK, but not between BK and des-Arg10-Kal. The BK response was decreased (5.09 +/- 0.30, N = 6 to 1.57 +/- 0.12, N = 7, P < 0.001) by the B2 receptor antagonist HOE 140 (0.1 microM, 15 min), while the B1 receptor antagonist des-Arg9-[Leu8]-BK (1 microM, 15 min) had no effect on BK or des-Arg10-Kal actions. Incubation of cells with Escherichia coli lipopolysaccharide (100 microg/ml, 24 h) alone or in association with tumor necrosis factor-alpha (TNF-alpha) (10 ng/ml, N = 6) did not enhance B1 agonist responses. BK was inhibited by repeated cell washouts in zero Ca++ solution (2.04 +/- 0.19, N = 6 P < 0.001), and the residual response was almost abolished by thapsigargin (Thaps) a sarcoplasmic reticulum (SR) calcium-ATPase inhibitor (1 microM) (1.18 +/- 0.08, N = 5 P < 0.001). Additionally, BK was not inhibited by verapamil (50 microM), nifedipine (30 microM), Ni++ (300 microM) or La (10 microM). In conclusion, BK induces [Ca++]i in mouse MC mainly by B2 receptor activation. B1 receptors have a minor role in this phenomenon even in the presence of known B1 receptor synthesis inducers. Finally, BK mobilizes extracellular calcium sources and, to a lesser extent, intracellular Thaps-sensitive calcium stores. The ion channels involved in calcium influx remain to be detected.

Animals↗
PubMed1999

Endopeptidases (kininases) are able to hydrolyze kinins in tubular fluid along the rat nephron.

The activities of serine endopeptidase, prolyl endopeptidase and neutral endopeptidase were determined in tubular fluid collected from several portions of the rat nephron as well as in urine. The enzyme activities were measured by HPLC using bradykinin (BK) as substrate. Free residual peptides of BK obtained by the action of these enzymes on the locally produced BK were also determined. The endopeptidase activities were found to be present throughout the nephron. Equimolar fragments of BK were detected in the early proximal tubule (Arg(1)-Pro(7), Phe(8)-Arg(9), Arg(1)-Gly(4), Phe(5)-Arg(9), and BK), late proximal tubule (Arg(1)-Phe(5), Arg(1)-Pro(7), Gly(4)-Pro(7), Gly(4)-Arg(9), and BK), late distal tubule (Arg(1)-Gly(4), Phe(5)-Arg(9), Arg(1)-Phe(5), Ser(6)-Arg(9), Gly(4)-Arg(9), BK, and [des-Arg(9)]BK) and urine (Phe(8)-Arg(9), Phe(5)-Arg(9), Arg(1)-Phe(5), Ser(6)-Arg(9), Arg(1)-Pro(7), Gly(4)-Pro(7), Gly(4)-Arg(9), BK, and [des-Arg(9)]BK). Our data suggest that the endopeptidases and exopeptidases are secreted by the nephron. Early proximal tubules secrete angiotensin converting enzyme and neutral endopeptidase, differing from late distal tubules that produce prolyl endopeptidase, serine endopeptidase, carboxypeptidase, and also neutral endopeptidase. All enzymes detected along the rat nephron were found in the urine. The existence of endopeptidases and carboxypeptidase in the distal nephron may have a potential physiological role in the inactivation of the kinins formed by kallikrein in the kidney and also in the inactivation of additional peptides other than BK.

Amino Acids↗
PubMed1999

Phyllanthus niruri inhibits calcium oxalate endocytosis by renal tubular cells: its role in urolithiasis.

We investigated the in vitro effect of an aqueous extract of Phyllanthus niruri L. on a model of CaOx crystal endocytosis by Madin-Darby canine kidney cells. The extract exhibited a potent and effective non-concentration-dependent inhibitory effect on the CaOx crystal internalization. This response was present even at very high (pathologic) CaOx concentrations and no P. niruri L.-induced toxic effect could be detected. Biochemical analysis of culture media containing P. niruri L. did not provide any clues for the elucidation of the cellular pathways affected by this natural product. Although further studies are necessary for a better understanding of the role of P. niruri L. in urolithiasis, our findings show that this natural product could be an attractive alternative for the treatment of urinary stones.

Animals↗
PubMed1999

[Female mortality in the Municipality of São Paulo: quality of medical death certificates].

OBJECTIVE: To evaluate the quality of the medical certification of deaths of 10-49 year-old women, resident in the Southern region of the city of S. Paulo METHODS: The Puffer methodology was utilized to investigate the causes of death of all 10-49 year-old women, resident in the region, and deceased in the year 1989 (664 deaths in the total). The main causes of death in the original death certificates and the "new" causes of death arisen from the research were compared. The sensitivity and the kappa index were calculated. RESULTS: In some chapters of the International Classification of Diseases and Causes of Death, 9th Revision (CID-9), a high sensitivity was found: "Diseases of the Circulatory System" (91.9%), "Neoplasms" (89.7%) and "External Causes" (84.1 %). In some others, a very low sensitivity was found. The chapter "Mental Illnesses", with a 34.3 percent sensitivity only, must be mentioned. From 11 deaths originally classified in this chapter, 32 cases were found. In most of these "new" cases, the main cause of death was found to be alcoholism. The chapter "Complications of Pregnancy, Delivery and the Puerperium", also showed a low sensitivity (44.9%). The kappa index was found to be 0.63, which indicated a regular concordance. DISCUSSION: The quality of the medical certification of causes of death is still unsatisfactory in the studied area. This poor quality may affect negatively the interventions in the area of women's health, masking the severity of important problems

Adolescent↗
PubMed1998

Potassium and sodium intake and excretion in calcium stone forming patients.

OBJECTIVE: To determine mean potassium (K) intake and its correlation with urinary calcium (uCa) and citrate excretion, as well as uCa, sodium (Na), and K levels of calcium stone forming patients. We determined the K-rich foods most commonly consumed by these patients. DESIGN: Case-control. SETTING: University-affiliated outpatient renal Lithiasis Unit. PATIENTS AND CONTROLS: One hundred hypercalciuric calcium stone forming patients (CSF, 54 men/46 women), 37 with associated hypocitraturia, were sequentially enrolled in the study that was performed before the initiation of any care for their renal stones. The control group consisted of 100 age-matched healthy subjects (HS, 47 men/53 women) who were laboratory employees with no history of renal stones. INTERVENTION: The analyses consisted of a 3-day dietary record to determine the mean K and calcium (Ca) intakes, and a 24-hour urine sample with measurements of K, Ca, Na, and citrate. MAIN OUTCOME MEASURE: K and Na intake determined by dietary record. RESULTS: uCa and Na levels and the Na/K ratio were significantly higher for CSF versus HS (238 +/- 118 v 148 +/- 74 mg/24 hours, 238 +/- 100 v 181 +/- 68 mEq/24 hours, 6.6 +/- 3.5 v 5.1 +/- 2.3, respectively, P < .05). The mean citrate excretion was lower in CSF than in HS patients (410 +/- 265 v 530 +/- 240 mg/24 hours). Mean uCa did not differ between groups. CSF patients showed a higher sodium chloride intake compared with HS (14 +/- 4 vs 8 +/- 3 g/day). The mean Ca intake of CSF and HS were 559 +/- 327 and 457 +/- 363 mg/day, respectively. The mean K intake of CSF and HS were 58 +/- 17 and 51 +/- 27 mEq/day. A positive correlation was observed between uCa and urinary sodium (r = .40 and r = .65, P < .05), urinary potassium and urinary citrate (r = .25 and r = .53, P < .05), uCa and Na/K (r = .33 and r = .56, P < .05) respectively for CSF and HS. The following were the K-rich foods consumed at least once a day by these groups: beans (by 70% of CSF and 75% of HS), tomatoes (by 42% of CSF and 50% of HS), oranges (by 30% of CSF and 55% of HS), and bananas (by 42% of CSF and 23% of HS). CONCLUSION: Despite the consumption of K-rich foods at least once a day, the mean K intake by CSF patients was 58 mEq/day. This intake can still be considered to be low, although it meets recommended daily dietary allowance requirements. Therefore, we describe herein a population of CSF with high-Na intake and normal- to low-K intake, which may contribute to stone formation.

Adult↗
PubMed1998

Purification and characterization of angiotensin I-converting enzymes from mesangial cells in culture.

OBJECTIVE: Previous analysis of the angiotensin I-converting enzyme (ACE) gene in this laboratory showed that primary mesangial cells in culture are able to express ACE mRNA. Moreover, ACE is produced as an ectoenzyme and as a secreted form of the enzyme, indicating a potential effect of local angiotensin II production on glomerular microcirculation. The aim of this study was to purify and characterize the secreted and intracellular ACE forms from mesangial cells in culture. METHODS AND RESULTS: Medium from Wistar rats mesangial cells was collected (third passage), incubated for 20 h with RPMI without fetal bovine serum and concentrated 29 times in an Amicon concentrator. The concentrated medium was submitted to gel filtration on an AcA-34 column and two peaks (ACE1, mol. wt 130 000 and ACE2, 60000) with ACE on activity Hippuryl-His-Leu and Z-Phe-His-Leu were separated. The mesangial cells were collected and ACE enzyme was extracted using Triton X-114, followed by centrifugation and concentration. The supernatant was submitted to the same chromatography as described above and two peaks with ACE activity (ACEInt1, mol. wt 130000 and ACEInt2, 68000) were separated. The purified ACE were inhibited by enalaprilat and captopril, two potent competitive inhibitors of ACE and by EDTA, using Hippuryl-His-Leu as a substrate. The Km values were 2 mM for ACE1 and ACE2 and 3 mM for ACEInt1 and ACEInt2. The enzymes ACE1 and ACE2 presented an optimum pH of 8.0 and ACEInt1 and ACEInt2 an optimum pH of 7.5. CONCLUSION: The activities of full-length wild-type and N-domain ACE were characterized by the ratio of the hydrolysis of Z-Phe-His-Leu/Hippuryl-His-Leu, which was 1 and 4, respectively. The ratios found for ACE1, ACE2, ACEInt1 and ACEInt2 in the present study were similar to those described above, suggesting that mesangial cells, besides showing the presence of intracellular ACE, are able to secret both full-length wild-type ACE and N-domain ACE. Thus, they may potentially have an effect, not only on bradykinin and angiotensin I (ACE wild-type), but also on substance P, luteinizing hormone-releasing hormone and Met-enkephalin to interfere with glomerular haemodynamics and with the renal microcirculation.

Angiotensin I↗
PubMed1997

Alteration of cytosolic calcium induced by angiotensin II and norepinephrine in mesangial cells from diabetic rats.

To evaluate functional alterations of mesangial cells induced by diabetes (DMC), we observed the changes of cytosolic calcium ([Ca]i) in response to the vasoconstrictor agonists angiotensin II (Ang II) and norepinephrine (NOR). DMC were obtained from rats with streptozotocin-induced diabetes, cultured in normal medium and identified as mesangial cells (MC) in the third subculture. [Ca]i was measured using fura-2 as a fluorophore. Basal calcium levels (60 to 80 nM) in DMC were not different from control mesangial cells (CMC). The high glucose (30 mM) medium concentration reduced the response of CMC and DMC to Ang II and NOR. This was not an osmotic effect since mannitol did not alter these responses. When DMC were stimulated with Ang II, a desensitized response was always observed, with a transient variation of [Ca]i (N = 6, P < 0.05). In contrast, a non-desensitized response with a sustained pattern of [Ca]i increases was obtained in NOR-stimulated DMC. Therefore, the present results suggest that DMC show a modified response to stimulation of the Ang II receptor, which is expressed phenotypically in culture by desensitization. Furthermore, these alterations induced by diabetes environment in MC in vivo were maintained in vitro despite a long period (approximately 5 months) in which the cells were grown in normal culture medium.

Angiotensin II↗
PubMed1997

Nephrology, dialysis and transplantation in Brazil.

The European Renal Association welcomes this opportunity and feels that European nephrologists should be informed about the state of nephrology in South America, with which particularly our Latin colleagues maintain close cultural relationships. The following report on Nephrology in Brazil is a welcome addition to a series of reports designed to provide to European nephrologists a global view of nephrology. It is hoped that this is not misconstrued as a violation of nephrological Monroe doctrine.

Acute Kidney Injury↗
PubMed1997

Effects of long-term training on the progression of chronic renal failure in rats.

To evaluate the effects of long-term exercise on the progression of chronic renal failure (CRF), adult Munich-Wistar rats with 5/6 renal mass ablation were submitted to treadmill exercise for 30 min 5 times/wk for 60 d. Whole kidney function and glomerular hemodynamics, proteinuria, and glomerular sclerosis were evaluated in 4 groups: Control, Sham trained (Sham + Ex), rats submitted to 5/6 nephrectomy (CRF) and maintained sedentary, and rats with 5/6 nephrectomy and trained (CRF + Ex). The groups with chronic renal failure (sedentary and trained) presented a reduction in total glomerular filtration rate (GFR) and in renal plasma flow (RPF), accompanied by an increase in single nephron GFR (SNGFR) and glomerular plasma flow (QA). However, the CRF + EX group did not show the glomerular hypertension observed in the CRF group. Despite the normalization of glomerular hypertension, proteinuria and sclerosis index were not different from the CRF sedentary group. Physical training provoked a vasodilatation of efferent arterioles, which induced the normalization of glomerular hypertension. These results suggest that the reduction alone of glomerular hypertension induced by exercise does not prevent the progression of renal disease, indicating the participation of other associated factors in this experimental model.

Animals↗
PubMed1997

Angiotensin I-converting enzyme activity in tubular fluid along the rat nephron.

The activity of angiotensin I-converting enzyme (ACE) was determined in tubular fluid collected from several portions of the rat nephron and urine and in total and efferent arteriolar blood using hippuryl-L-His-Leu as substrate. ACE activity decreased 30% from the pre- to the postglomerular arterioles (P < 0.001), suggesting a role of the glomerulus in ACE clearance. The enzyme activity was found to be present throughout the rat nephron. However, the highest activities were found in the proximal tubule and urine (0.692 +/- 0.007 and 1.05 +/- 0.015 pmol x microl(-1) x min(-1), respectively). Compared with other segments, ACE activity decreased from the initial portion of the proximal tubule to the distal nephron and increased again in the urine. Along the proximal tubule, ACE was secreted and degraded and/or reabsorbed and then secreted again into the collecting duct; no ACE activity was found in the late distal tubule, but a high level was detected in the urine, indicating a potential physiological role in the inactivation of the kinins formed by kallikrein beyond the connecting tubules. Moreover, the possible role of mesangial cells (MC) in the decrease of intraglomerular ACE was also evaluated. The analysis of ACE gene showed that MC in culture are able to express ACE mRNA. Moreover, ACE is produced as an ectoenzyme and as a secreted form of the enzyme, indicating a potential effect of local angiotensin II production on MC function.

Animals↗
PubMed1997

Heterogeneity of glomerular perfusion and filtration induced by epinephrine and norepinephrine.

The role of catecholamines in the distribution of intrarenal blood flow and in single-nephron glomerular filtration rate (SNGFR) was evaluated in anesthetized Wistar rats by the Hanssen technique. Epinephrine (EPI) and norepinephrine (NOR) were infused to produce elevations of 20-30 mmHg in mean arterial pressure. Superficial and juxtamedullary nephron perfusion and filtration were determined by the presence of Prussian blue dye. In the control group, 100% of the nephrons presented a homogeneous pattern of perfusion and filtration. In contrast, a heterogeneous distribution of the dye was found even in the larger arteries (arciform and radial), indicating variable perfusion and filtration in both superficial and juxtamedullary nephrons. The effects of EPI and NOR were also evaluated in the superficial cortex by the micropuncture technique in two additional groups of Munich-Wistar rats. Mean SNGFR was 27% and 54% lower in the EPI- and NOR-treated groups, respectively. No change in mean intraglomerular hydraulic pressure was observed after EPI or NOR infusion in spite of a highly scattered pattern, indicating an important variability in perfusion along the superficial cortex, and/or different sensitivity of the pre- and post-glomerular arterioles. The present data suggest that EPI and NOR may affect intrarenal hemodynamics by modifying perfusion and filtration in both superficial and juxtamedullary glomeruli and not by shifting blood flow from superficial to juxtamedullary nephrons. The heterogeneous pattern of perfusion was a consequence of differential vasoconstriction along the intrarenal arteries, probably due to different density and/or sensitivity of the adrenergic receptor subtypes present in the intrarenal vascular tree.

Animals↗
PubMed1997

Nephrotoxicity of acyclovir and ganciclovir in rats: evaluation of glomerular hemodynamics.

Whole-kidney function and glomerular hemodynamics were evaluated after acute (50 mg/kg, iv, in bolus) and short-term chronic (50 mg mg/kg, ip, 5 days) acyclovir (ACV) and short-term chronic ganciclovir (Gan; 30 mg/kg, ip, 5 days) treatment in envolemic Munich-Wistar rats. The evaluation of whole-kidney function of the ACV groups showed a significant reduction in total GFR (0.96 +/- 0.10 to 0.28 +/- 0.02 mL/min in the acute group, P < 0.05, and 1.04 +/- 0.09 to 0.33 +/- 0.04 mL/min in the chronic group, P < 0.05) with a marked increase in total renal vascular resistance (TRVR) (33 +/- 5 to 122 +/- 26 mm Hg.min/mL in the acute group and 28 +/- 3 to 74 +/- 18 mm Hg.min/mL in the chronic group, P < 0.05) and a reduction in RPF (2.29 +/- 0.25 to 0.81 +/- 0.15 mL/min in the acute group and 2.57 +/- 0.36 to 1.30 +/- 0.40 mL/min in the chronic group, P < 0.05). Conversely, urinary flow (V') was unchanged (3.6 +/- 0.4 to 3.6 +/- 0.2 microL/min in the acute group) or elevated (3.7 +/- 0.6 to 6.6 +/- 1.4 microL/min in the chronic group, P < 0.05). The evaluation of glomerular hemodynamics after ACV treatment showed a reduction in single-nephron GFR (SNGFR) (46.4 +/- 5.3 to 26.2 +/- 3.4 nL/min in the acute group and 38.7 +/- 5.7 to 21.1 +/- 5.7 nL/min in the chronic group, P < 0.05), a significant elevation in total arteriolar resistance (RT) (2.90 +/- 0.44 to 4.94 +/- 0.77 x 10(10) dyn.s.cm-5 in the acute group and 3.72 +/- 0.45 to 9.00 +/- 2.40 x 10(10) dyn.s.cm-5 in the chronic group, P < 0.05) and a severe reduction in glomerular plasma flow rate (QA) (152.6 +/- 29.5 to 103.8 +/- 27.8 nL/min in the acute group and 149.1 +/- 29.8 to 68.5 +/- 10.0 nL/min in the chronic group, P < 0.05). However, the glomerular ultrafiltration coefficient, Kf, was changed only in the chronic group (0.1002 +/- 0.0165 to 0.0499 +/- 0.0090 nL/(s.mm Hg), P < 0.05). After Gan treatment, no changes were observed in GFR (1.04 +/- 0.09 to 0.96 +/- 0.08 mL/min, with the maintenance of RPF (2.57 +/- 0.36 to 2.66 +/- 0.34 mL/min) and a nonsignificant reduction in TRVR (28 +/- 3 to 20 +/- 3 mm Hg.min/mL. The short-term Gan treatment also showed a different pattern in glomerular hemodynamics by inducing an elevation in SNGFR (38.7 +/- 5.7 to 50.3 +/- 2.8 nL/min, P < 0.05) with no changes in QA (150 +/- 30 to 135 +/- 22 nL/min) and a mild vasodilation, RT (3.7 +/- 0.5 to 2.7 +/- 0.3 x 10(10) dyn.s.cm-5, P < 0.05) associated with an increment in Kf (0.1002 +/- 0.0165 to 0.2400 +/- 0.0700 nL/(s.mm Hg), P < 0.05). Thus, ACV induced acute renal failure by reducing GFR and SNGFR by an increase in TRVR and RT with a reduction in RPF and QA. Also, after short-term treatment with ACV, a reduction in Kf led to a reduction of SNGFR. On the other hand, Gan treatment did not induce acute renal failure by the adopted techniques.

Acute Kidney Injury↗
PubMed1997

Rhabdomyolysis due to hyperosmolarity leading to acute renal failure.

Authors present the case of a 37-year-old man admitted to the emergency room of Universidade Federal de São Paulo-Escola Paulista de Medicina, with hyperosmolar coma, following progressive muscle discomfort and loss of renal function, with further need of dialysis therapy. Initial laboratory evaluation showed marked hyperglycemia, hypernatremia, hyperosmolarity, and high levels of creatinine. In the evolution he presented an elevation of creatino-phosphokinase levels in parallel with increasing levels of urea and creatinine. Urinalyses showed progressive increase in proteinuria and hematuria. A muscle biopsy was performed and confirmed the presence of muscular necrosis. The purpose of this paper is to emphasize hyperosmolarity as a newly described cause of rhabdomyolysis. The authors point out its multifactorial physiopathology and also stress the relatively common occurrence of acute renal failure (ARF) following an episode of rhabdomyolysis, and the poor prognosis that this complication represents.

Acute Kidney Injury↗
PubMed1997

Nephrotoxicity of low-osmolality contrast media.

To evaluate renal function after the use of a low-osmolality radiological contrast medium (CM), we prospectively analyzed 39 patients submitted to the following examinations: arteriography (n = 32), phlebography (n = 3), computed tomography (n = 3), angioplasty (n = 1), and retrograde pyelography (n = 1). The patients were divided into three groups: group 1, control, formed by renal donors (CT, n = 11 and 11 exams); group 2, hypertensive patients (HYPT, n = 15 and 16 exams); and group 3, patients with diseases of multiple etiologies (MIX, n = 13 patients and 13 exams). Additionally, the patients were divided according to their renal function into: group 4, with a moderate deficit of renal function, creatinine clearance (CrCl) 25 to 60 mL/min (n = 15 patients and 15 exams); and group 5, with a mild deficit of renal function, CrCl > or = 60 mL/min (n = 14 patients and 14 exams). The CM utilized was ioxaglic acid (Hexabrix) the incidence of acute renal failure (ARF) among the patients studied was 12.5% (5/40), and CrCl was the best parameter to monitor the alterations in renal function, which occurred in 35% of the patients, although the changes were mild, reversible, and did not need any therapeutic interventions. The triggering of ARF in these patients may have been due to multiple factors presented at time of CM examination. Thus, it is not possible to identify a single risk factor. However, it is probable that previous important impairment of renal function was the most expressive risk factor.

Acute Kidney Injury↗
PubMed1997

Neurohumoral systems in patients with cirrhosis.

In order to evaluate the activation of the sympathetic nervous and renin-angiotensin systems and antidiuretic hormone release in the setting of chronic liver disease, we studied 30 patients with cirrhosis who presented normal renal function. The cirrhotic patients were divided into two groups according to Child's score: 20 were Child A and 10 Child B. The control group consisted of 10 normal subjects. Blood samples were collected for determination of norepinephrine (NE), dopamine (DA), angiotensin I and II (AI and AII), and antidiuretic hormone (ADH), using the method of high-performance liquid chromatography (HPLC). No significant differences (p < 0.05) were found in the plasma levels of NE, DA, AI, and AII between the cirrhotic patients and the controls, although the absolute values observed in both groups of cirrhotics were clearly higher than in controls. The ADH levels were higher in Child B in comparison to Child A patients and controls, though this difference was not significant as well. Our results suggest a hormonal activation in cirrhotic patients, even in the early stages of hepatic disease (without ascites). We also noted an increase in ADH levels in Child B patients in relation to Child A and controls, although there was no difference in osmolality, suggesting a non-osmotic ADH release.

Adult↗