Journal of Nephrology & Therapeutics

Introduction: In order to minimize the risk of hyperkalemia (hK+) in patients with heart failure (HF), in 2005 and 2009 ACC/AHA (American College of Cardiology; American Heart Association) joint guidelines recommended associating renin-angiotensin system (RAS) inhibition with low-dose ALD-block in patients with serum creatinine (sCr) less than 2.5 mg/dl and serum potassium (sK+) lower than 5 mEq/l. A prevalence of HF in individuals aged 65 and over with mild renal failure at risk of hyperkalemia is steeply increasing. Such data has persuaded us to analyze the association between over-65 HF standard treatment and hK+.

Aim: This observational retrospective study analyzed emergency room admissions aged 65 and over undergoing ACEI with ALD-block or potassium sparing diuretics (K+-sparing) and hK+ (sK+ > 6 mEq/l) over a one year period, from January to December 2010.

Methods: 8,407 over-65 emergency admissions of 62,348 adult entries have been selected from the hospital database. Data was matched with the Local Medical District pharmaceutical database with joint use of ACEI and ALDblock or K+-sparing medications. Acute Kidney Injury (AKI) was defined according to AKIN (Acute Kidney Injury Criteria) guidelines.

Results: ACEI with spironolactone or K+-sparing was found in 332 (3.9%) out of the 8,407 over-65 emergency admissions. Seven HF patients (2.1% aged 79-82, 5F 2M) of 332 had hK+ (sK+, 6.3-8.5 mEq/l). Six patients had spironolactone and 1 K+-sparing treatment. sCr before admission was available in 3 (sCr, 1.1-1.4 mg/dl) out of 7 patients, all of which developed AKI. All 7 patients with hK+ received conservative medical treatment only.

Conclusions: hK+ occurred in 7 (2.1%) out of the 332 HF over-65 emergency admissions on ACEI. It might suggest a strict application of the current ACC/AHA guidelines with a closer follow-up for those HF patients at risk of developing AKI and hK+.

Objectives: This study was conducted to evaluate upper digestive endoscopic lesions among patients with chronic kidney disease.

Methodology: We conducted a retrospective cross-sectional study in Nephrology and Gastroenterology services at Hospital Center University Aristide Le Dantec from January 2008 to December 2009. All patients with chronic kidney disease who underwent an upper gastrointestinal endoscopy were included.

Results: Fifty patients were included, with a mean age of 44.2 years and a sex ratio (male/female) of 1.27. Upper digestive endoscopy was abnormal in 76%. Peptic esophagitis was noted in 7 patients, hiatal hernia in 10 and cardial incontinence in 2. Congestive gastritis was observed in 6 cases, followed by erosive and hemorrhagic gastritis in 5 cases each one and a gastric ulcer in 2. Six patients presented a bulbitis, which was erosive in 3, congestive in 2 and 1 of the large folds. Bulbar ulcer was noted in 3 patients and post bulbar ulcer was also noted in 3 patients. One patient presented a congestive duodenitis.

Conclusion: Upper digestive endoscopy lesions are frequent and diverse among patients with chronic kidney disease. These finding justify the systematization of upper digestive endoscopy in digestive complaining uremic patients.

Urine analysis is used as a diagnostic method is lauded by many a nephrologists through the ages as equivalent to a liquid biopsy. The urine sample is easy to procure and is a physiological process and pain less. It has a wide and varied use as a diagnostic tool as in follow up, confirmation of diagnosis and screening measures. The question of the hour is do automated machines find themselves in the bracket of adequateness do they do justice for all the elements present in a pathological urine specimen. For example spermatozoa, trichomomas, schistosomiasis, ectoparasites however the WBCs and RBCs can be reported in a qualitative manner which compare well and unequivocal without much ado but is it all!

Background: Metformin has been a main stay medication in the treatment of type 2 diabetes mellitus. However, its use has been limited by its potential risk of metabolic acidosis in chronic kidney disease. Although this been anecdotally proposed, there have been no studies suggesting the effects of metformin in end stage renal failure, especially in the setting of peritoneal dialysis. We submit a case of metformin inadvertently used in end stage renal failure, without evidence of metabolic acidosis.

Case presentation: A 54 year old man with known type 2 diabetes mellitus presented late to our service with end stage renal failure. He had been on metformin at time of diagnosis of end stage renal failure. Although initially ceased on admission, metformin was inadvertently restarted on discharge from another hospital where he had been transferred for a tenchkoff catheter insertion. This issue was only realised 10 days later following an incidental medication review. He had already commenced peritoneal dialysis at this stage. He was asymptomatic and there was no evidence of metabolic acidosis. We hypothesise that Metformin use in end stage renal failure with dialysis may not be as harmful. To our knowledge, this is the first case report suggesting the use of metformin in such a setting.

Conclusion: Metformin has long been associated with the potential adverse effect of metabolic acidosis. However, our case report suggests further investigation into the potential use of metformin in end stage renal failure requiring dialysis, particularly those requiring peritoneal dialysis. In light of its overwhelming beneficial mortality effects, further studies would need to confirm the safety of such measures, including the need for a creation of an international registry.

All substances with molecular weights up to 58 kDa retained in the blood as the results of renal dysfunction are potential uremic toxins. The search for endogenous toxic compounds seems to offer a novel approach to identifying and explaining any so far unexplored specific effects on the body organs and systems. In contemporary laboratory diagnostics there are no suitable markers for use in comprehensive evaluation of complex toxicity of uremic compounds accumulated in successive stages of developing renal dysfunction. To provide a sound basis for treatments which would effectively protect against or slow down multiple organ injury caused by uremic toxins novel parameters are needed, more specific than urea and creatinine. Identification of reliable biomarkers or their panels needs careful consideration of their concentrations in biological materials, biological activity and usefulness for effective diagnosis. Classification of uremic compounds, based on their chemical properties, role in pathophysiological processes and the organs where they are formed remains to be elucidated with meticulous observation of clearly formulated rules guiding the process.