ABSTRACT
Diabetes is the leading cause of chronic kidney disease (CKD), which makes estimation of renal function crucial. Serum creatinine is not an ideal marker of glomerular filtration rate (GFR), which also depends on digestive absorption, and the production of creatinine in muscle and its tubular secretion. Formulas have been devised to estimate GFR from serum creatinine but, given the wide range of GFR, proteinuria, body mass index and specific influence of glycaemia on GFR, the uncertainty of these estimations is a particular concern for patients with diabetes. The most popular recommended formulas are the simple Cockcroft-Gault equation, which is inaccurate and biased, as it calculates clearance of creatinine in proportion to body weight, and the MDRD equation, which is more accurate, but systematically underestimates normal and high GFR, being established by a statistical analysis of results from renal-insufficient patients. This underestimation explains why the MDRD equation is repeatedly found to give a poor estimation of GFR in patients with recently diagnosed diabetes and is a poor tool for reflecting GFR decline when started from normal, as well as the source of unexpected results when applied to epidemiological studies with a 60mL/min/1.73m(2) threshold as the definition of CKD. The more recent creatinine-based formula, the Mayo Clinic Quadratic (MCQ) equation, and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) improve such underestimation, as both were derived from populations that included subjects with normal renal function. Determination of cystatin C is also promising, but needs standardisation.
Subject(s)
Diabetic Nephropathies/diagnosis , Diabetic Nephropathies/physiopathology , Kidney Function Tests/methods , Models, Biological , Biomarkers/metabolism , Diabetic Nephropathies/metabolism , HumansABSTRACT
The importance of fibroblast growth factor 23 (FGF 23) has been highlighted in the mechanism of urinary leakage of phosphate in the oncogenic osteomalacia (OO). It is now a component of diagnosis of this disease. We report a 58-year-old man who presented with osteomalacia and hypophosphatemia secondary to urinary leakage of phosphorus. Although serum FGF 23 was normal, the diagnosis of OO was obtained after another cause of acquired prolonged hypophosphatemia has been excluded (hyperparathyroidism and Fanconi syndrome in particular). The search for a deep tumor was performed, allowing the detection of a 12 mm hemangiopericytoma in the upper thigh. Its removal allowed the rapid resolution of clinical symptoms and laboratory abnormalities. The importance of functional sequelae in OO depends on prompt diagnosis. Tumorectomy remains the optimal treatment. Thus, the search for a secreting tumor is essential even in the absence of elevated serum FGF 23.
Subject(s)
Fibroblast Growth Factors/biosynthesis , Neoplasms, Connective Tissue/diagnosis , Fibroblast Growth Factor-23 , Humans , Male , Middle Aged , Osteomalacia , Paraneoplastic SyndromesABSTRACT
AIM: The National Kidney Foundation recommends stratification of renal failure into moderate (Glomerular Filtration Rate: GFR = 30-60 mL/min/1.73 m2), severe (15-30) or terminal (<15) using the Cockcroft-Gault (CG) or the Modification of Diet in Renal Disease (MDRD) equations. We studied the biases in these methods in an attempt to improve the standard CG (MCG) and devise a strategy for stratification. METHODS: GFR was measured by 51Cr-EDTA clearance in 200 diabetic patients: 100 (Group 1: study of concordance) before 2003 and 100 thereafter (Group 2: validation of MCG). The CG was modified by replacing body weight by its mean value: 76. RESULTS: In group 1, the recommended equations only correctly stratified 50 patients. The CG, not the MDRD, underestimated GFR if BMI was normal, and overestimated it in obese patients. In group 2, the MCG was well correlated with GFR and not biased by weight. Over the whole population, the MCG and MDRD were more accurate for the diagnosis of moderate and severe renal failure. The MDRD showed the lowest differences with GFR, except if GFR > 60, where the MCG performed better. All formulae overestimated low GFR, the MDRD also underestimated high GFR. The best stratification (147/200) was obtained using the MCG if creatininemia < 120 micromol/l and the MDRD if creatininemia > or =120 micromol/l. CONCLUSION: The CG is biased by weight, the MCG corrects this. The more accurate MDRD cannot be used in all patients as it underestimates high GFR. The best stratification was obtained using the MCG at low and the MDRD at high creatininemia.
