Prethivee Nagarajan

Rare occurrence of fatal Candida haemulonii peritonitis in a diabetic CAPD patient.

Abstract A 68-year-old diabetic chronic kidney disease patient on continuous ambulatory peritoneal dialysis for two years developed Candida haemulonii peritonitis without any predisposing factors. There is no effective treatment for this fungus. A peritoneal biopsy showed morphological changes of acute inflammation and chronicity.

Mineral bone disease in maintenance hemodialysis patients: Association with morbidity and mortality.

There is a paucity of data on mineral bone disease in maintenance hemodialysis (MHD) patients from India. This retrospective analysis was undertaken on 858 (males: 599; females: 259) patients from two medical centers on MHD from 1998 to 2010. Age, gender, months on dialysis, hours per session of dialysis, hemoglobin, serum calcium, inorganic phosphorus, intact parathyroid hormone (iPTH), urine output, erythropoietin dosage per week, blood sugar, blood pressure, urea reduction rate, gain in fluid and fluid removed per session, serum albumin, alkaline phosphatase, vitamin D level, supplemental vitamin D and use of phosphate binder for therapy were documented. Overall, 191 patients died (22%) during the observation period. There was an 86% patient survival rate at 1 year on dialysis and an overall predicted 3-year survival rate of 78%. A relatively higher iPTH (P = 0.012), a need for vitamin D supplementation (P = 0.003), less hours on dialysis per session (P = 0.046) and a non-vegetarian diet (P = 0.022) were significantly associated with mortality.

Is there a genetic predisposition to new-onset diabetes after kidney transplantation?

Kidney transplant recipients may develop new-onset diabetes after transplantation (NODAT) and transplant-associated hyperglycemia (TAH) (NODAT or new-onset impaired glucose tolerance-IGT). We studied 251 consecutive renal transplant South Asian recipients for incidence of NODAT and its risk factors between June 2004 and January 2009. Pre-transplant glucose tolerance test (GTT) identified non-diabetics (n = 102, IGT-24, NGT-78) for analysis. Baseline immunosuppression along with either cyclosporine (CsA) (n = 70) or tacrolimus (Tac) (n = 32) was given. Patients underwent GTT 20 days (mean) post-transplant to identify NODAT, normal (N) or IGT. TAH was observed in 40.2% of the patients (40% in CsA and 40.6% in Tac) (P = 0.5). NODAT developed in 13.7% of the patients (12.9% in CsA and 15.6% in Tac) (P = 0.5). Overall, Hepatitis C (P = 0.007), human leukocyte antigen (HLA) B52 (P = 0.03) and lack of HLA A28 (A68/69) (P = 0.03) were associated with TAH. In the Tac group, higher Day 1 dosage (P <0.001), HLA A1 (P = 0.04), B13 (P = 0.03) and lack of DR2 (P = 0.004) increased the risk of TAH. In the CsA group, HLA A10 (P = 0.03), failure of triglyceride (P = 0.001) or low-density lipoprotein (LDL) (P = 0.03) to lower or high-density lipoprotein to rise (P = 0.001), and higher post-transplant LDL (P <0.001) and cholesterol levels (P = 0.02) were associated with NODAT or TAH. Post-transplant fasting plasma glucose on Day 1 had sensitivity-54.5%, specificity-50.1%, positive predictive value-18.1% and negative predictive value-84.8% for detecting NODAT. In conclusion, there is a genetic predisposition to NODAT and TAH in South Asia as seen by the HLA associations, and a predisposition exists to the individual diabetogenic effects of Tac and CsA based on HLA type. This could lead to more careful selection of calcineurin inhibitors based on HLA types in the South Asian population.

Optimal management of hyperphosphatemia in end-stage renal disease: an Indian perspective.

There has been an exponential increase in the incidence of diabetes and hypertension in India in the last few decades, with a proportional increase in chronic kidney disease (CKD). Preventive health care and maintenance of asymptomatic chronic disease such as CKD are often neglected by patients until they become symptomatic with fluid retention and uremia. Management of hyperphosphatemia in CKD remains one of the challenges of nephrology in India for this reason, as it is almost completely asymptomatic but contributes to renal osteodystrophy, metastatic vascular calcification, and acceleration of cardiovascular disease. Lack of understanding of the dangers of asymptomatic hyperphosphatemia, the huge pill burden of phosphate binders, difficulty with dietary and dialysis compliance, and most importantly, the added expense of the drugs places additional road blocks in the treatment of hyperphosphatemia at a population level in developing countries like India. In this review we seek to address the contribution of hyperphosphatemia to adverse outcomes and discuss economic, cultural, and societal factors unique to the management of phosphate levels in Indian patients with advanced CKD.

Progressive pulmonary hypertension: Another criterion for expeditious renal transplantation

The aim of this retrospective study was to compare the prevalence of pulmonary hypertension in a cohort of patients with end-stage renal disease (ESRD) prior to and following renal transplantation and to identify the possible risk factors. Of the 425 renal transplantations performed between 2001 and 2007, Doppler echocardiographic findings were available in 124. The echocardiographic data, collected both pre- and post-transplant, included the pulmonary artery pressure (PAP), ejection fraction and left ventricular hypertrophy. The data analyzed included age, gender, hypertension, diabetes, smoking status, along with blood urea, creatinine, glomerular filtration rate, hemoglobin, hemodialysis duration, urine albumin, arterio-venous access and body mass index (BMI). Chi-square test was used for discrete variables and ANOVA was used for continuous variables. Of the patients studied, males comprised 72%; the mean age was 43.3 ± 13.02 years; 87% were hypertensive, 30% were diabetic and 4% were smokers. Statistical analysis revealed a significant reduction of the PAP, irrespective of its severity, following renal transplantation (P <0.05). The PAP had no significant correlation with any of the parameters analyzed, with the exception of BMI (P <0.05). Our study suggests that the PAP gets reduced in patients with ESRD after renal transplantation.

Diagnostic dilemma of ultrafiltration failure in a continuous ambulatory peritoneal dialysis patient.

A 42-year-old male with chronic kidney disease (CKD), stage 5 on continuous ambulatory peritoneal dialysis (CAPD) using a swan-neck double-cuff Tenckhoff catheter presented with abdominal pain, vomiting, nausea and reduced appetite for 1 month, along with a poor dialysate outflow and ultrafiltration failure (< 400mL/day) for 20 days. As stated by the patient, dialysate effluent was clear. Abdominal examination was unremarkable. After a 6-hour dwell, the dialysate showed a leucocyte count of 0.17 x 109/L (170 cells) with 0.75 (75%) neutrophils and 0.24 (24%) lymphocytes, Gram stain negative, acid-fast bacilli (AFB) smear negative and no growth on Lowenstein and Jensen culture medium. The Mantoux test done was unremarkable. Blood urea nitrogen was 12 mmol/L (33 mg/dL), serum creatinine 954 μmol/L (10.8 mg/dL), hemoglobin (Hb) 88 g/L (8.8 g/dL), erythrocyte sedimentation rate (ESR) 140 mm/hr, serum albumin 24 g/L(2.4 g/dL), electrolytes were normal. As the outflow was slow, an erect X-ray of the abdomen showed migration of the catheter (Figure 1), and a laproscopic examination showed intraperitoneal catheter with fibrinous exudates and adhesions (Figure 2), which were released. A peritoneal biopsy was done that showed granuloma with Langhans’ type giant cell suggestive of tuberculosis (Figure 3), and the biopsy specimen stained with Ziehl Neelsen stain showed acid-fast tubercle bacillus (Figure 4). A computed tomography (CT) of the chest showed left basal pulmonary scarring, small calcified right apical nodule, and calcified mediastinal nodules suggestive of pulmonary tuberculosis sequelae. The patient was initiated on rifampicin 450 mg OD, pyrazinamide 750 mg BID, ciprofloxacin 500 mg BID, isoniazid 150 mg OD, along with vitamin B6. Dialysate flow and ultrafiltration improved 7 days after starting the medication and the dialysate cell count returned to normal.

Enterobacter cloacae osteomyelitis induced post-infectious glomerulonephritis on diabetic nephropathy with progressive renal failure.

Infection has been well documented to cause glomerulonephritis (GN), with Streptococcus being the most common pathogen. However, the pattern of the disease has changed over recent decades [1–3]. The bacterial flora now comprises Staphylococcus and Gram-negative strains, and the focus of infection is wider than the throat and the skin [1]. GN secondary to osteomyelitis has rarely been reported. We report a case of immune complex-mediated diffuse proliferative GN with acute on chronic renal failure, superimposed on diabetic nephropathy due to osteomyelitis caused by Enterobacter cloacae.