ISRN nephrology最新文献

Aim. The prevalence of chronic kidney disease (CKD) as a serious public health problem is growing in the elderly. This study aimed to assess CKD prevalence and its related risk factors in elderly population of Fars province. Methods. In this cross sectional study a total of 1190 elderly people are enrolled, and demographic and medical data were obtained. Data were analyzed by SPSS, and P of less than 0.05 was considered as statistically significant. Results. Prevalence of CKD stages III-V was 27.5% in the 60-69 years age group, 36.5% in the 70-79 years age group, and 40% in the ≥80 years age group. The prevalence of CKD increased with ageing in both men and women. Female gender was the strongest risk factor for CKD. Conclusions. Prevalence of CKD in elderly is high in Southern Iran, which has become an important health problem while it can be prevented or delayed in progression.

Background. The role of gender for nephroprotectant agent such as vitamin E in cisplatin- (CP-) induced nephrotoxicity has not been documented yet. Methods. One group from each gender of Wistar rats received a single dose of CP (7 mg/kg; i.p) and was treated with vitamin E (1 g/kg/day) for 7 days, and they were compared with similar gender in the control group. Results. The serum levels of blood urea nitrogen (BUN) and creatinine (Cr) in male animals treated with CP was not different from the control group, but it was significantly different in the female rats (P < 0.05). The CP-induced damage intensity in male kidney tissue was not significantly different between the CP-treated and control groups, but this was not the case in female, indicating that the tissue damage in female is significantly different from the control group (P < 0.05). No significant difference in serum levels of magnesium (Mg), nitrite, malondialdehyde (MDA), and lactate dehydrogenase (LDH) was seen between the genders. Kidney weight and body weight changes were statistically significant in both genders (P < 0.05). Significant difference was observed in uterus weight between the two groups of female (P < 0.05). Conclusion. Vitamin E may prevent CP-induced nephrotoxicity in male, but possibly it has not such nephroprotectant effect in female.

Background. Low serum magnesium has been associated with an increased cardiovascular risk in the general population and in dialysis patients. Our aim was to analyze the influence of serum magnesium on overall mortality and cardiovascular outcomes in patients with advanced CKD not yet on dialysis. Methods. Seventy patients with CKD stages 4 and 5 were included. After a single measurement of s-magnesium, patients were followed a mean of 11 months. Primary end-point was death of any cause, and secondary end-point was the occurrence of fatal or nonfatal CV events. Results. Basal s-magnesium was within normal range (2.1 ± 0.3 mg/dL), was lower in men (P = 0.008) and in diabetic patients (P = 0.02), and was not different (P = 0.2) between patients with and without cardiopathy. Magnesium did not correlate with PTH, calcium, phosphate, albumin, inflammatory parameters (CRP), and cardiac (NT-proBNP) biomarkers but correlated inversely (r = -0.23; P = 0.052) with the daily dose of loop diuretics. In univariate and multivariate Cox proportional hazard models, magnesium was not an independent predictor for overall mortality or CV events. Conclusions. Our results do not support that serum magnesium can be an independent predictor for overall mortality or future cardiovascular events among patients with advanced CKD not yet on dialysis.

Since time immemorial uroscopic analysis has been a staple of diagnostic medicine. It received prominence during the middle ages with the introduction of the matula. Urinary discoloration is generally due to changes in urochrome concentration associated with the presence of other endogenous or exogenous pigments. Observation of urine colors has received less attention due to the advances made in urinalysis. A gamut of urine colors can be seen in urine bags of hospitalized patients that may give clue to presence of infections, medications, poisons, and hemolysis. Although worrisome to the patient, urine discoloration is mostly benign and resolves with removal of the offending agent. Twelve urine bags with discolored urine (and their predisposing causes) have been shown as examples. Urine colors (blue-green, yellow, orange, pink, red, brown, black, white, and purple) and their etiologies have been reviewed following a literature search in these databases: Pubmed, EBSCO, Science Direct, Proquest, Google Scholar, Springer, and Ovid.

We here present the results of ultrasonographic (US) evaluations on the alteration of renal diameter of chronic HD patients. Of 109 outpatient HD patients who had neither severe acquired cystic disease of the kidney nor hereditary polycystic kidney disease, we performed US two or three times to measure their maximum renal diameter (mean of both kidneys), and the yearly alteration rate was calculated. The average interval of the two measurements was 35.9 months, and the average HD duration from the HD induction to the first measurement was 29.5 months. The average decrease rate of renal diameter was 4.34 ± 0.4 (SE) mm/year. No statistical difference was seen on the decrease rate in relation to gender, age and original disease (among three groups, glomerulonephritis and IgA nephropathy, diabetes, and others including hypertension). However, the decrease rate was large when the first measurement was close to the induction of hemodialysis, suggesting that the alteration rate reduced according to the hemodialysis vintage (5.3 ± 0.8 mm/year, first measurement not more than 10 months after induction of HD and 1.5 ± 1.6 mm/year, first measurement more than 80 months after induction of HD). Renal diameter decreased approximately 4.3 mm each year, and the decrease rate slowed as the length of time on dialysis increased.

Guanylin peptides (GPs) family includes guanylin (GN), uroguanylin (UGN), lymphoguanylin, and recently discovered renoguanylin. This growing family is proposed to be intestinal natriuretic peptides. After ingestion of a salty meal, GN and UGN are secreted into the intestinal lumen, where they inhibit sodium absorption and induce anion and water secretion. At the same conditions, those hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis and therefore prevent hypernatremia and hypervolemia after salty meals. In the intestine, a well-known receptor for GPs is guanylate cyclase C (GC-C) whose activation increases intracellular concentration of cGMP. However, in the kidney of GC-C-deficient mice, effects of GPs are unaltered, which could be by new cGMP-independent signaling pathway (G-protein-coupled receptor). This is not unusual as atrial natriuretic peptide also activates two different types of receptors: guanylate cylcase A and clearance receptor which is also G-protein coupled receptor. Physiological role of GPs in other organs (liver, pancreas, lung, sweat glands, and male reproductive system) needs to be discovered. However, it is known that they are involved in pathological conditions like cystic fibrosis, asthma, intestinal tumors, kidney and heart failure, obesity, and metabolic syndrome.

Diabetes Insipidus (DI) is either due to deficient secretion of arginine vasopressin (central) or to tubular unresponsiveness (nephrogenic). Drug induced DI is a well-known entity with an extensive list of medications. Polyuria is generally defined as urine output exceeding 3 liters per day in adults. It is crucial to identify the cause of diabetes insipidus and to implement therapy as early as possible to prevent the electrolyte disturbances and the associated mortality and morbidity. It is very rare to have an idiosyncratic effect after a short use of a medication, and physicians should be aware of such a complication to avoid volume depletion. The diagnosis of diabetes insipidus is very challenging because it relies on laboratory values, urine output, and the physical examination of the patient. A high clinical suspicion of diabetes insipidus should be enough to initiate treatment. The complications related to DI are mostly related to the electrolyte imbalance that can affect the normal physiology of different organ systems.

Background. Nitric oxide (NO) concentration in serum is altered by cisplatin (CP), and NO influences CP-induced nephrotoxicity. The effect of nephroprotectant agent supplementation (vitamin E, human recombinant erythropoietin (EPO), or n-acetylcysteine (NAC)) on the NO metabolites levels after CP administration in the two genders was determined. Methods. Sixty-four adult Wistar rats were randomly divided into 10 groups. Male and female rats in different groups received vehicle (saline), CP (7 mg/kg) alone, CP plus EPO (100 IU/kg), CP plus vitamin E (250 mg/kg), and CP plus NAC (600 mg/kg). CP was administrated as a single dose, but the supplementations were given for a period of 7 days. Results. In male rats, the serum levels of total NO metabolites (NO x ) and nitrite were increased significantly (P < 0.05) by CP. However, vitamin E significantly reduced the serum levels of these metabolites, which was increased by administration of CP (P < 0.05), and such findings were not observed for female rats. The EPO or NAC did not influence NO metabolites neither in male rats nor in female rats. Conclusion. Although vitamin E, EPO, and NAC are reported to be nephroprotectant agents against CP-induced nephrotoxicity, only vitamin E could reduce the level of all NO metabolites only in male rats.

To identify differences in treatment and outcome of various types of glomerulonephritis developing in the course of infections triggering antineutrophil cytoplasmic antibody (ANCA) formation, we analyzed published reports of 50 patients. Immunosuppressives were added to antibiotics in 22 of 23 patients with pauci-immune glomerulonephritis. Improvement was noted in 85% of 20 patients with information on outcomes. Death rate was 13%. Corticosteroids were added to antibiotics in about 50% of 19 patients with postinfectious glomerulonephritis. Improvement rate was 74%, and death rate was 26%. Two patients with mixed histological features were analyzed under both pauci-immune and post-infectious glomerulonephritis categories. In 9 patients with other renal histology, treatment consisted of antibiotics alone (7 patients), antibiotics plus immunosuppressives (1 patient), or immunosuppressives alone (1 patient). Improvement rate was 67%, permanent renal failure rate was 22%, and death rate was 11%. One patient with antiglomerular basement disease glomerulonephritis required maintenance hemodialysis. Glomerulonephritis developing in patients who became ANCA-positive during the course of an infection is associated with significant mortality. The histological type of the glomerulonephritis guides the choice of treatment. Pauci-immune glomerulonephritis is usually treated with addition of immunosuppressives to antibiotics.

Introduction. The mortality and morbidity associated with acute kidney injury (AKI), unfortunately, remain unacceptably high. We aimed to detect the extent of serum neutrophil gelatinase-associated lipocalin (NGAL) to early detect AKI in critically ill children. Subjects and Methods. This is a case control study. It included 75 subjects that include 15 as controls and 60 critically ill children. Patients were further subdivided according to RIFLE criteria into two other categories: patients who developed AKI and patients who did not develop AKI. Serum NGAL assayed on admission and after 3 days. Results. There was significant increase in the level of NGAL among patients group when compared with control group. Also, 21.7% of children admitted to PICU developed AKI from which 8.3% needed dialysis. The receiver operating characteristic curve of NGAL at day 0 revealed AUC of 0.63 with 95% CI of 0.50-0.77. At a cutoff value of 89.5 ng/mL, the sensitivity of NGAL was 84.6%, while specifcity was 59.6%, positive predictive value was 36.7%, negative predictive value was 68.4%, and accuracy was 93.3% in diagnosis of AKI. Conclusion. We found that NGAL acts as a sensitive marker rather than a specific one for AKI. At the same time, it presents as a negative predictive value more valuable than being a positive predictive value in detecting AKI.