Diabetic nephropathy and membranous nephropathy can both present with nephrotic syndrome. Here, we report on a 43-year-old female patient suffering from type 1 diabetes, diabetic retinopathy, arterial hypertension, and nephrotic syndrome. Blood glucose levels were poorly controlled by a basal-bolus insulin regimen as shown by an HbA1c of 15.9% (150 mmol/mol). The concomitant antihypertensive medication consisted of an angiotensin-2 receptor blocker, a β-blocker, a calcium antagonist, and furosemide. In March 2012, her serum creatinine and urine albumin-to-creatinine ratio were 1.06 mg/dL and 7 g/g, respectively. Until December 2012, both serum creatinine and albuminuria increased to 1.9 mg/dL and 11 g/g urinary creatinine, respectively. The estimated glomerular filtration rate via the MDRD-2 formula (Modification of Diet in Renal Disease) declined from 56 to 28 mL/min/1.73 m2. Furthermore, she presented with aggravated leg oedemas, hypoalbuminemia of 2.4 mg/dL, hypertriglyceridemia, and hypertension reflecting nephrotic syndrome. …
Diuretics are among the most commonly prescribed medications and, due to their mechanisms of action, electrolyte disorders are common side effects of their use. In the present work we investigated the associations between diuretics being taken and the prevalence of electrolyte disorders on admission as well as the impact of electrolyte disorders on patient outcome.In this cross sectional analysis, all patients presenting between 1 January 2010 and 31 December 2011 to the emergency room (ER) of the Inselspital, University Hospital Bern, Switzerland were included. Data on diuretic medication, baseline characteristics and laboratory data including electrolytes and renal function parameters were obtained from all patients. A multivariable logistic regression model was performed to assess the impact of factors on electrolyte disorders and patient outcome.A total of 8.5% of patients presenting to the ER used one diuretic, 2.5% two, and 0.4% three or four. In all, 4% had hyponatremia on admission and 12% hypernatremia. Hypokalemia was present in 11% and hyperkalemia in 4%. All forms of dysnatremia and dyskalemia were more common in patients taking diuretics. Loop diuretics were an independent risk factor for hypernatremia and hypokalemia, while thiazide diuretics were associated with the presence of hyponatremia and hypokalemia. In the Cox regression model, all forms of dysnatremia and dyskalemia were independent risk factors for in hospital mortality.Existing diuretic treatment on admission to the ER was associated with an increased prevalence of electrolyte disorders. Diuretic therapy itself and disorders of serum sodium and potassium were risk factors for an adverse outcome.
Hyponatremia is a disorder of water homeostasis. Water balance is maintained by the collaboration of renal function and cerebral structures, which regulate thirst mechanisms and secretion of the antidiuretic hormone. Measurement of serum-osmolality, urine osmolality and urine-sodium concentration help to diagnose the different reasons for hyponatremia. Hyponatremia induces cerebral edema and might lead to severe neurological symptoms, which need acute therapy. Also, mild forms of hyponatremia should be treated causally, or at least symptomatically. An inadequate fast increase of the serum sodium level should be avoided, because it raises the risk of cerebral osmotic demyelination. Basic pathophysiological knowledge is necessary to identify the different reasons for hyponatremia which need different therapeutic procedures.
In experimental transplant models, upregulation of renal heat shock proteins (HSP) represents a new therapeutic tool to improve allograft survival. In this clinical study, we hypothesized that HSP-72 expression in pretransplant donor kidney biopsies predicts posttransplant outcome. Expression of HSP-72 in pretransplant biopsies was assessed by immunohistochemistry and in situ hybridization in 82 consecutive renal transplantations and clinical data were collected prospectively during the first six months posttransplant. Renal tubular expression of HSP-72 was low and not influenced by donor-, graft-, or procedure-related risk factors. Neither strength nor pattern of pretransplant HSP-72 staining discriminated allografts with complicated (40%) posttransplant courses from those without complications (60%). The low HSP-72 expression in pretransplant donor kidney biopsies failed to predict delayed graft function or acute rejection. These findings suggest that constitutive HSP-72 gene expression at the time of engraftment does not play a role in graft protection.
