Diabetes prevalence is increasing worldwide, mainly due to the increase in type 2 diabetes. Diabetic nephropathy occurs in up to 40% of people with type 1 or type 2 diabetes. It is important to identify patients at risk of diabetic nephropathy and those who will progress to end stage renal disease. In clinical practice, most commonly used markers of renal disease and progression are serum creatinine, estimated glomerular filtration rate and proteinuria or albuminuria. Unfortunately, they are all insensitive. This review summarizes the evidence regarding the prognostic value and benefits of targeting some novel risk markers for development of diabetic nephropathy and its progression. It is focused mainly on tubular biomarkers (neutrophil-gelatinase associated lipocalin, kidney injury molecule 1, liver-fatty acid-binding protein, N-acetyl-beta-d-glucosaminidase), markers of inflammation (pro-inflammatory cytokines, tumour necrosis factor-α and tumour necrosis factor-α receptors, adhesion molecules, chemokines) and markers of oxidative stress. Despite the promise of some of these new biomarkers, further large, multicenter prospective studies are still needed before they can be used in everyday clinical practice.

In clinical practice the glomerular filtration rate (GFR) is estimated from serum creatinine-based equations like the Cockcroft-Gault formula (C&G) and Modification of Diet in Renal Disease formula (MDRD). Recently, serum cystatin C-based equations, the newer creatinine formula (The Chronic Kidney Disease Epidemiology Collaboration formula (CKD-EPI)), and equation that use both serum creatinine and cystatin C (CKD-EPI creatinine & cystatin formula) were proposed as new GFR markers. Present study compares serum creatinine-based equations, combined (including both serum creatinine and cystatin C) equation, and serum simple cystatin C formula (100/serum cystatin C) against 51CrEDTA clearance in 113 adult overweight Caucasians with diabetes mellitus type 2 (DM2) and chronic kidney disease (CKD). The results of present study demonstrated that the simple cystatin C formula could be a useful tool for the evaluation of renal function in overweight patients with DM2 and impaired kidney function in daily clinical practice in hospital and especially in outpatients. Despite the advantages of the simple cystatin C formula, cystatin C-based equations cannot completely replace the “gold standard” for estimation of the GFR in a population of DM2 patients with CKD, but may contribute to a more accurate selection of patients requiring such invasive and costly procedures.

Background: Serum cystatin C (SCC)-based formulas and the newer creatinine formula (the Chronic Kidney Disease Epidemiology Collaboration formula (CKD-EPI)) were proposed as improved glomerular filtration rate (GFR) markers. The aim of our study was to compare serum creatinine (SCr)-based and SCC-based equations against 51Cr-EDTA clearance in patients with mildly to moderately impaired kidney function. Methods: 255 adult Caucasian patients with chronic kidney disease (GFR 89–30 ml/min/1.73 m2) were enrolled. In each patient, 51Cr-EDTA clearance, SCr and SCC were determined. GFR was calculated using the Cockcroft-Gault (C&G), Modification of Diet in Renal Disease (MDRD), CKD-EPI formulas and simple cystatin C formula (SCCF) (100/SCC). Results: The receiver-operating characteristic curve analysis (cut-off for GFR 60 ml/min/1.73 m2) showed that the SCCF had a higher diagnostic accuracy than C&G but not than MDRD or CKD-EPI formulas. The Bland-Altman analysis for the same cut-off value showed that creatinine formulas underestimated and SCCF overestimated the measured GFR. Analysis of ability to correctly predict a patient’s GFR 60 ml/min/1.73 m2 showed the higher ability for the SCCF compared to all creatinine-based formulas. Conclusion: Our results indicate that the SCCF is a reliable marker of GFR and comparable to creatinine formulas including the CKD-EPI formula.

Presentations of abdominal pain in patients on peritoneal dialysis deserve maximal attention and careful differential diagnosis on admittance to medical care. In this case report a gangrenous appendicitis in a patient on automated peritoneal dialysis is presented. We report the case of a 38-year-old Caucasian man with end-stage renal disease who was on automated peritoneal dialysis and developed acute abdominal pain and cloudy peritoneal dialysate. Negative microbiological cultures of the peritoneal dialysis fluid and an abdominal ultrasonography misleadingly led to a diagnosis of culture negative peritonitis. It was decided to remove the peritoneal catheter but the clinical situation of the patient did not improve. An explorative laparotomy was then carried out; diffuse peritonitis and gangrenous appendicitis were found. An appendectomy was performed. Myocardial infarction and sepsis developed, and the outcome was fatal. A peritoneal dialysis patient with abdominal pain that persists for more than 48 hours after the usual antibiotic protocol for peritoneal dialysis-related peritonitis should immediately alert the physician to the possibility of peritonitis caused by intra-abdominal pathology. Not only peritoneal catheter removal is indicated in patients whose clinical features worsen or fail to resolve with the established intra-peritoneal antibiotic therapy but, after 72 hours, an early laparoscopy should be done and in a case of correct indication (intra-abdominal pathology) an early explorative laparotomy.