Clinical and experimental nephrology
-
Clin. Exp. Nephrol. · Dec 2003
Case ReportsDeep venous thrombosis, myocardial infarction, and occlusion of vascular access associated with heparin-induced thrombocytopenia in a diabetic hemodialysis patient.
We report a patient with diabetic endstage renal disease with an initial platelet count of 17.6 x 10(4)/mm3 who developed type-II heparin-induced thrombocytopenia (HIT) during the induction period of hemodialysis (HD) when unfractionated heparin was used. Because the recognition of the condition and the treatment of this patient with HIT was unsatisfactory, she developed deep venous thrombosis, myocardial infarction, and occlusion of vascular access, at times of platelet counts of 4.1 x 10(4), 7.7 x 10(4), and 6.4 x 10(4)/mm3, respectively, with antibodies to heparin/platelet factor 4 complex. Unfortunately, we misjudged in our belief that the thromboembolic events might be associated with an underlying procoagulant state in diabetic nephrotic syndrome, rather than being associated with the clinical picture of HIT. This case report suggests that the clinician must consider HIT in the differential diagnosis for thromboembolic complications during the induction period of HD, because unfractionated heparin is the major anticoagulant used in HD.
-
Clin. Exp. Nephrol. · Sep 2003
Comparative Study Clinical Trial Controlled Clinical TrialEffects of the angiotensin II type 1 receptor antagonist candesartan, compared with angiotensin-converting enzyme inhibitors, on the urinary excretion of albumin and type IV collagen in patients with diabetic nephropathy.
We previously reported that the angiotensin II type 1 receptor antagonist candesartan was effective in reducing blood pressure and microalbuminuria in hypertensive patients with diabetic nephropathy after angiotensin-converting enzyme (ACE) inhibitors were replaced due to side effects. In the present study, the clinical effects of candesartan were investigated and compared with ACE inhibitors in patients with stage 2 or 3A diabetic nephropathy, mainly with respect to the effects on the urinary excretion of albumin and type IV collagen. ⋯ It was revealed that ACE inhibitors and candesartan reduced urinary albumin excretion to a similar extent in patients with diabetic nephropathy. From the results of the present study, it is inferred that the renoprotective effect of candesartan in diabetic nephropathy may partially differ from that of ACE inhibitors.
-
Clin. Exp. Nephrol. · Jun 2003
Case ReportsA simple quantitative approach to analyzing the generation of the dysnatremias.
Although the dysnatremias are the most common electrolyte disorders in hospitalized patients, the complexity of the parameters normally used to explain their generation mechanistically is often bewildering to medical students and experts alike. A number of methods have been utilized clinically to analyze retrospectively and predict prospectively the pathogenesis of these disorders. These approaches include the measurements of plasma and urine osmolality, free water clearance, electrolyte free water clearance, and tonicity balance. ⋯ The conceptual simplification resulting from the use of this formula should significantly improve the current approaches used in analyzing the generation of the dysnatremias.
-
Clin. Exp. Nephrol. · Jun 2003
Case ReportsA new quantitative approach to the treatment of the dysnatremias.
Rapid correction of the dysnatremias can result in significant patient morbidity and mortality. To avoid overly rapid correction of the dysnatremias, the sodium deficit equation, water deficit equation, and Adrogue-Madias equation are frequently utilized to predict the change in plasma sodium concentration (Delta[Na+]p) following a therapeutic maneuver. However, there are significant limitations inherent in these equations. ⋯ These equations consider the mass balance of Na+, K+, and H2O, as well as therapy-induced changes in TBW. The first equation is applicable to both hypernatremia and hyponatremia. The second equation is applicable to the management of severe symptomatic SIADH requiring intravenous therapy.
-
There have been significant advances recently in the understanding of the molecular causes of nephrogenic diabetes insipidus. The resistance of the collecting duct to the action of vasopressin in this disorder results from abnormalities in several of the intricate steps that mediate the increase in principal cell hydraulic conductivity in response to the hormone. In this article, we review the current understanding of the known genetic causes of nephrogenic diabetes insipidus that affect the binding of vasopressin to the V2 receptor and subsequent intracellular signaling events, as well as the translocation of aquaporin-2 water channels to the apical membrane. In addition, genetic diseases, which decrease collecting-duct water absorption by diminishing the interstitial medullary osmolarity, are discussed.