Contrast-induced nephropathy (CIN) is one the most important renal complications following contrast injection in percutaneous coronary intervention. We compared the protective effect of normal saline (NLS), Ringer's lactate (RL), and sodium bicarbonate (Bi). In this study, patients with coronary angiography indication were divided into three groups by simple randomization method: NLS, RL, and Bi solution groups. Creatinine (Cr) alterations, glomerular filtration rate, and urine pH were evaluated prior and after the procedure. Data were analyzed with SPSS and P value less than 0.05 was taken as significant. In this study, 300 patients [150 men (50%), mean age 59.1 ± 10.6 years] were studied. The CIN incidence overall was 10% (30 patients): 8.3% (8 patients) in NLS; 16.5% (17 patients) in RL; and 5% (5 patients) in Bi group. It was significantly different among three groups (P = 0.018), and CIN incidence was significantly lower in Bi vs. RL group (P = 0.012). Baseline Cr clearance was higher in patients who developed CIN (78.4 ± 26.0 vs. 69.8 ± 21.6 mL/dL, P = 0.044). Urine pH after trial in CIN group was lower than the patients without CIN (5.5 ± 1.4 vs. 6.3 ± 1.8 mL/dL, P = 0.024). Higher urine pH and its change during study were seen in Bi group (P < 0.05). Cr at the initiation of study and the use of RL vs. Bi may be prognostic factors in CIN progression (P < 0.002). Sodium barcarbonate as fluid had more protective effect than NSL or RL on prevention of CIN in patients undergoing coronary angiography. The risk factors for CIN in our study were higher baseline serum Cr and use of RL as hydration fluid.

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Of all cases of idiopathic steroid-sensitive nephrotic syndrome (NS) in children, 40%–75% cases need long-term continuous steroids and/or other immunosuppressants to maintain remission, the effects of which on growth and renal function remain an issue of concern. The study aimed at exploring the safety and efficacy of mycophenolate mofetil (MMF) as a remission-maintaining agent in children with a diagnosis of frequent relapsing or steroid-dependent NS (FRNS/SDNS) requiring continuous medication for at least 1 year. Thirty-two children thus included received MMF (1000–1200 mg/m²/day) for 7 months along with tapering doses of oral prednisolone if it was being given from before with an attempt at tapering at 0.25 mg/kg/month ultimately stopping it altogether. Individuals were followed up for at least 5 more months after stopping MMF. Out of 32 children, 26 had SDNS and 6 had FRNS with male:female ratio being 2.2:1. The mean standard deviation (± SD) age of onset of disease was 2.72 ± 1.3 years and that entry to the study was 7.17 ± 2.2 years. Significant fall in number of relapses was observed following the introduction of MMF (110 in pre-MMF12 month period vs. 52 in post-MMF 12 months [p = 0.002]). The mean relapse rate/year/patient also decreased from 3.43 ± 1.26 to 1.62 ± 1.14 after entry in the study. Significant reduction of the cumulative dose of steroid regarding mean ± SD of mg/kg/year was also found following the introduction of MMF (190.9 ± 47.81 vs. 119.09 ± 60.09 [p = 0.001]). MMF is an efficacious agent in maintaining remission and reducing steroid requirement in children with FRNS and SDNS.

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Systemic lupus erythematosus (SLE) and myasthenia gravis (MG) are two autoimmune diseases that have a higher incidence in young females, relapsing–remitting course, and positive antinuclear antibodies. SLE and MG are two different clinical syndromes, which can coexist or precede each other; however, their occurrence in the same patient is rare. We report a 38-year-old female with biopsy-proven lupus nephritis on steroids and cyclophosphamide, later developed MG. Nerve conduction studies showed the decremental response of 15%–25% over facial muscles with no decremental response over limb muscles. Although antianticholinesterase receptor (AchR) antibodies were negative, she was treated with oral pyridostigmine 60 mg twice daily and clinical improvement of ocular symptoms was seen within 48 h. At present, she is on oral prednisolone and mycophenolate mofetil with follow-up creatinine of 1.4 mg/dl and no neurological symptoms.

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Dengue is a growing public health problem in India, and acute kidney injury (AKI) is one of the least studied complications of dengue virus infection (DVI). This study was conducted to investigate the incidence, clinical characteristics, and risk factors for AKI in DVI. This was a retrospective study of patients with confirmed DVI presenting as dengue fever (DF) or dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) at our center over a period of 2 years. A total of 620 subjects fulfilling inclusion criteria were studied. Patients were divided into two cohorts (90 patients with AKI and 530 patients without AKI) to determine independent predictors of AKI. Among 620 patients, 454 (73.22%) had classical DF, 141 (22.74%) patients had DHF, and 25 (4.03%) patients had DSS. AKI was present in 90 (16.36%) patients; approximately one-third (31, 34.45%) had AKIN stage 1, 33 (36.66%) patients had AKIN stage 2, and 26 (28.88%) had AKIN stage 3. Among those with AKI, 14 patients expired and all had DHF/DSS. On multivariate logistic regression, AKI was associated with male gender [odds ratio (OR): 2.9], DHF (OR: 7.9), rhabdomyolysis (OR: 8.2), multiple-organ dysfunction (OR: 18.2), hypertension (OR: 0.7), diabetes mellitus (OR: 4.8), delayed hospitalization (OR: 2.2), and use of nephrotoxic drugs (OR: 2.86). In all, 320 patients (51.61%) had hospital stay >3 days. We found that AKI was an independent predictor for longer duration of hospital stay (OR: 7.2, 95% confidence interval: 4.8–10.7). AKI in DVI is associated with significant morbidity, mortality and longer hospital stay.

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Hypercalcemia rarely causes acute pancreatitis due to secretory block in the pancreas and damage by accumulated proteases. Hypercalcemia, though described in granulomatous disorders, is uncommon in tuberculosis. Acute kidney injury is known to occur with acute pancreatitis, secondary to sepsis and septic shock; however, acute pancreatitis resulting in acute cortical necrosis is very rare. We report a 22-year-old woman, who presented with pain abdomen and vomiting. She was found to have features of acute pancreatitis, both biochemically and radiologically. She had hypercalcemia on presentation and this was attributed to be the cause for pancreatitis as other causes were ruled out. 1, 25-dihydroxyvitamin D level was high with normal parathyroid hormone level. Whole-body positron emission tomography-computed tomography showed increased fluorodeoxyglucose uptake in the terminal ileum and histology from that area showed noncaseating granuloma with acid-fast bacilli in the tissue. She was treated with antituberculosis therapy; hypercalcemia improved over a period of time and pancreatitis resolved. She developed anuric renal failure, and kidney biopsy showed patchy acute cortical necrosis. She is dialysis dependent at the end of 6 months. To the best of our knowledge, this is the first case report of a patient with ileal tuberculosis presenting with hypercalcemia and acute pancreatitis. This case is reported due to the rarity of extrapulmonary tuberculosis presenting with symptomatic hypercalcemia, acute pancreatitis, and acute renal cortical necrosis.

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Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive disorder that is caused by mutation in genes coding for tight junction proteins claudin-16 and claudin-19. It is characterized by renal wasting of magnesium and calcium associated with the development of nephrocalcinosis and renal stones by early childhood. Most of them progress to end-stage renal failure by the second or third decade. Here, we report two siblings with FHHNC, who presented with nephrocalcinosis without any extrarenal manifestations, one of them having novel homozygous nonsense mutation in claudin-16 (CLDN16) (c.620G>A, p. Trp207Ter). Both were treated with dietary changes, hydrochlorothiazide, potassium citrate, and magnesium supplementation. FHHNC is a rare cause of nephrocalcinosis, and we believe that it should be considered in the presence of nephrocalcinosis with hypercalciuria and hypomagnesemia.

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Sickle cell disease (SCD) is a hereditary hemoglobinopathy characterized by abnormal hemoglobin production which leads to hemolytic anemia and intermittent occlusion of small blood vessels, which further leads to tissue ischemia, chronic organ damage, and organ dysfunction including urinary system. To measure the serum levels of cystatin-C and beta 2 microglobulin in pediatric patients with SCDand to investigate their significance as early biomarkers of glomerular and/or renal tubular dysfunction. This study was conducted among 70 children with SCD and 40 age and sex-matched children as a control group. All subjects underwent a full medical history, through physical examination, laboratory investigations including blood urea, serum creatinine, serum ferritin, estimated glomerular filtration rate (eGFR) using the Schwartz formula, creatinine clearance, urinary albumin/creatinine ratio, serum cystatin-C, and β-2 microglobulin levels. Pediatric patients with SCD had significantly higher serum cystatin-C and β-2 microglobulin levels compared to controls. In addition, serum cystatin-C and β-2 microglobulin levels were positively correlated with blood urea, serum creatinine, serum ferritin, urinary albumin/creatinine ratio, duration of iron chelating agents and frequency of blood transfusion/year. Serum cystatin-C and β-2 microglobulin levels were negatively correlated with hemoglobin. Our data concluded that serum cystatin-C and β-2 microglobulin had highersensitivity and specificity (91%, 90% and 85.7%, 100%, respectively) than serum creatinine (79% and85%, respectively).Serum Cystatin-C and β-2 microglobulin are early specific and sensitive biomarkers for evaluating glomerular and tubular dysfunction in children with SCD.

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Chronic fluid overload as well as excessive fluid removal are associated with increased morbidity and mortality in hemodialysis (HD) patients. The clinical method to probe the dry weight is often inaccurate and the bioimpedance spectroscopy (BIS) is shown to improve the accuracy. We compared the impact of BIS and clinical methods to guide ultrafiltration (UF) in a randomized controlled study on the intradialytic complications and blood pressure control in prevalent HD patients. Fifty patients on maintenance HD were randomized to BIS method (BIS-group) and clinical method (CL-group) to guide UF. The body composition monitor (BCM) was done post-HD in all patients at baseline and 2-weeks interval during the study period of 6 months to determine the hydration status, but the result was revealed only to the nephrologist managing the patients in BIS-group to probe the dry weight. The endpoints of the study were blood pressure control, intradialytic complications and anti-hypertensive drug burden. The mean age was 56.0 ± 12.0 years and 70% were male. There was significant increase in patients with normal hydration in BIS-group (20% vs. 88%, p = 0.0001), but remained similar to baseline in CL-group (40% vs. 48%, p = 0.3) at 6 months. The incidence of intradialytic hypotension was significantly reduced in BIS-group (4.84 ± 3.0 vs. 2.8 ± 3.13 events/patient/6 months, p = 0.003). There was 35% reduction in hypertensive pill burden in BIS-group with similar blood pressure, compared to CL-group. Post-dialysis underhydration was more common than over or normal hydration at baseline in our population, indicating that clinical method to probe dry weight often resulted in hypovolemia. BIS method to determine dry weight resulted in normalization in volume status and consequently resulted in significant reduction in intradialytic hypotension and anti-hypertensive pill burden over 6-month period.

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Hemodialysis remains the most common mode of renal replacement therapy in patients with end-stage renal disease (ESRD). It requires an appropriate vascular access. The vascular access while being the “lifeline” for patients on hemodialysis is also the “Achilles' heel” of the therapy. Although the gold standard for vascular access remains an arteriovenous fistula, in clinical practice situations often arise which mandates the use of central venous catheter (CVC). These CVCs while providing an immediate access for the performance of hemodialysis may be associated with various complications. These complications are usually minor requiring conservative management, but at times may be potentially life-endangering. We report a case where during the placement of the dialysis catheter, it inadvertently perforated the left innominate vein. A potential disaster was prevented by deploying a covered stent over the site. This alternative percutaneous approach when available can be a safe alternative to open surgical intervention and represents a paradigm shift in our approach.

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Diabetic muscle infarction (DMI) is one of the unusual complications of poorly controlled diabetes. It is usually seen in association with other microvascular complications. This condition is reported rarely, probably due to it's under recognition. It is also seen in patients with chronic kidney disease and should be considered in patients presenting with acute onset of limb pain. Here we present two cases of DMI in dialysis patients and discuss the available literature to highlight the clinical characteristics of the cases. We also present a diagnostic algorithm to discuss evaluation of dialysis patients presenting with limb pain.

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Monoclonal gammopathy of undetermined significance does not have end organ damage, but a proportion of cases manifest with renal injury when it is called monoclonal gammopathy of renal significance (MGRS). Herein, we describe a case of acute hepatitis E infection, which precipitated the development of MGRS. The patient underwent kidney biopsy for elevated creatinine with clinical suspicion of drug-induced interstitial nephritis. On light microscopy, there were periodic acid–Schiff negative-fractured casts in tubules with giant cell reaction around them. The tubular epithelial cells showed intracytoplasmic bile pigment. On direct immunofluorescence, casts showed kappa restriction. A diagnosis of bilirubin proximal tubulopathy and light chain cast nephropathy was made, and possibility of myeloma was suggested. On further evaluation, κ:λ ratio was 27, β2 microglobulin was 8036 ng/ml, and bone marrow examination showed 5% plasma cells. There were no bony lesions, and serum calcium was 8.6 mg/dl. The present case is unique in two aspects. First, the patient developed MGRS triggered by acute hepatitis E in less than a month. Second, the MGRS lesion was manifested in the form of light chain cast nephropathy.

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There are many factors involved in the delayed graft function of a renal graft, with prolonged cold ischemia time being one of the most relevant. The aim of this study is to evaluate the relationship between the time of cold ischemia and the delayed graft function, and acute rejection and graft loss at 1 year of follow-up. A retrospective cohort of 347 renal transplant patients were evaluated during the years 2009–2013. The incidence of delayed graft function was 18.4% (n = 65). The cold ischemia time was an independent risk factor for delayed graft function (odds ratio [OR] 1.10, 95% confidence interval [CI] 1.04–1.16). By grouping the time of cold ischemia by intervals, the risk of delayed graft function was greater in the 12–18 hours group (OR 2.06, 95% CI 1.02–4.15) and in the >18 hours group (OR 3.38, 95% CI 1.57–7.27). The risk of acute rejection did not increase with longer cold ischemia (p = 0.69), and cold ischemia time was not a risk factor for renal graft loss at 1-year follow-up (hazard ratio 0.97, 95% CI 0.88–1.06). In conclusion the time of cold ischemia (>12 hours) in renal transplant recipients of optimal deceased donors increases the risk of delayed graft function; however, this does not negatively impact the results in acute rejection or graft loss in the first year of the transplant.

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A 63-year-old diabetic gentleman with microvascular complications presented with advanced azotemia and anemia. He was stabilized with blood transfusion and hemodialysis. With the probable diagnosis of diabetic nephropathy-related end-stage renal disease, he underwent kidney transplantation. He had delayed graft function. Graft biopsy done on the 2^nd postoperative day showed acute tubular necrosis. Graft biopsy repeated after 2 weeks for persistent graft dysfunction showed myeloma cast nephropathy (MCN) and light chain proximal tubulopathy. Work-up for multiple myeloma was positive. He was started on plasmapheresis and chemotherapy. However, he suffered sudden cardiac death during dialysis after 1 week. The presence of MCN in the early graft biopsy implies that it must have been the cause for his native kidney failure. Thus, renal failure in a diabetic should not always be presumed to be due to diabetic nephropathy, and kidney biopsy should be done in diabetics with atypical features.

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