Diabetes, Hypertension and Kidney Disease Combination "DHKD Syndrome" is common in India.

Objectives: The study was designed to find out frequency of (i) Diabetes mellitus (DM) as a cause Chronic Kidney Disease (CKD), (ii) Association between diabetic-CKD (diabetic patients who subsequently developed CKD as complication), hypertension (HT) and obesity. Further assessment was made to (iii) Identify percentage of diabetics attending medical and nephrology OPD had prior testing for proteinuria and or creatinine. Methods: After ethical consideration this prospective observational study was conducted on consecutive 6175 patients who gave consent to participate in two major referral hospitals one in Delhi and other in Bhubaneswar (BBSR). Primary hypertension was defined as blood pressure of ≥140/90 mmHg detected before onset of DM or detected together in the absence of CKD (elevated serum creatinine S Cr ≥1.7 mg/dL and or proteinuria > 0.3g/24H). Upper limit of serum creatinine was kept at 1.7 mg for this study. Mean value of three estimations on different days was recorded. Detail clinical history of DM and HT was taken. Body Mass Index (BMI), ocular fundi examination, urine analysis, serum creatinine, lipid profile, blood glucose, HbA1C tests were conducted in all patients. They were regularly followed up in renal clinic at about 2 month interval for repeat investigations. Blood pressure in nondiabetic-CKD patients was recorded for comparison. Further, consecutive diabetic patients attending general medicine OPD for first time were examined, their previous investigations were carefully scrutinized and recorded. Urine for albuminuria and serum creatinine were tested every month over a period of one year. Results: In Delhi diabetic-CKD was observed in 68.4% and the same was 56.2% in BBSR giving a combined figure of 62.3 percent. On close analysis of past record primary hypertension was observed in 75.4% who subsequently developed diabetes and CKD. Frequency of association between diabetic-CKD and HT were 88.2% and 69.3% in two cities respectively, combined frequency being 78.7 percent. Association of diabetic-CKD and obesity was 55.1 % and 55.9% in two cities respectively with combined frequency of 55.5 percent. In contrast obesity in non-diabetic-CKD patients in Delhi and BBSR was found in 43.1% and 18.5% respectively, combined frequency being 30.8%. Fifty four percent of diabetic patients who attended medical OPD for the first time were found to have proteinuria and elevated serum creatinine. However, they were not earlier tested for those parameters. Hence, they were unaware of CKD. Conclusion: Diabetes was found to be a bigger cause (62.3%) of CKD than what has been reported thus far in India. At presentation association of diabetic-CKD with HT was recorded higher (78.7%) in India. Hence use of the syndrome "DHKD", (complex of diabetes, hypertension and kidney disease) is justifiable. Our study shows 54.4% of diabetic patients attending medicine OPD were uninvestigated by either physician or GP for CKD because urine albumin and serum creatinine tests were lacking. Thus, progression to CKD in many patients went unnoticed. Syndromic diagnosis of "DHKD" therefore in our view is important to create general awareness for early detection and effective treatment of diabetic nephropathy.

Unresolved issues and current concepts in management of primary glomerulonephritis.

The successful treatment of primary glomerulonephritis (GN) presenting with nephrotic syndrome in adults depends heavily on an accurate diagnosis. A successful diagnosis depends on a correct approach, combining light microscopy, immunofluorescence, and other special staining of renal biopsy material examined by a trained nephropathologist. A good clinical history and serological tests easily rule out possible secondary causes (for example, infection, autoimmune, metabolic or toxic) in most cases. Unfortunately, these procedures are not put into practice in most cases in developing countries, resulting in missed diagnosis and unnecessary steroid and immunosuppressant therapy with its inherent morbidity. Following the emergence of IgA and IgM nephropathies as very common forms of glomerular disorders in some countries, immunofluorescence has become absolutely necessary for their diagnosis. Moreover, a recent meta-analysis has defined different treatment protocols for minimal change nephropathy, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy for a better outcome. This article emphasizes and elaborates on these issues for proper management of primary GN.

Etoricoxib-induced life-threatening hyperkalemia and acute kidney dysfunction against the background of telmisartan and a low sodium diet.

Drug-induced hyperkalemia is not uncommon and may be life-threatening when presenting acutely in the emergency department. We present a case of severe hyperkalemia precipitated acutely by etoricoxib in a patient who was on telmisartan and a low sodium (potassium chloride-rich) diet. A 75-year-old male with a past medical history of well-controlled diabetes and hypertension was prescribed etoricoxib (90 mg daily) for 3 days for musculoskeletal backache. He had been taking his routine medications including telmisartan and a potassium-rich salt substitute for many years, without any recent change in dosage or quantity. There was evidence of microalbuminurea; however, the renal functions and electrolytes prior to starting etoricoxib were normal. He presented to the emergency department with signs and symptoms of life-threatening hyperkalemia (serum potassium 7.7 mEq/dl), accelerated hypertension, congestive heart failure, pulmonary edema and acute renal failure. Acute medical management and withholding all drugs that could cause hyperkalemia improved his serum potassium levels over 24 h and renal parameters within 5 days. All the other drugs except etoricoxib were restarted under observation over 8 weeks with no recurrence of the acute episode. Non-steroidal analgesics and other COX-2 inhibitors (rofecoxib and celecoxib) have been known to precipitate renal failure and hyperkalemia specially in patients at risk for the same; although not unexpected, this may be the first reported case of life-threatening hyperkalemia precipitated by etoricoxib in a previously stable patient having increased risk of renal failure and hyperkalemia.