Publications by authors named "Jagannath Saikumar"

Background: Treatment of heart failure with reduced ejection fraction (HFrEF) requires guideline-directed medication therapy (GDMT) consisting of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker in combination with an indicated beta-blocker. There is concern that end-stage renal disease (ESRD) patients are not being prescribed GDMT. The study aim was to determine whether outcomes differ for patients with HFrEF and ESRD receiving GDMT compared to those not receiving GDMT.

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Rhabdomyolysis is a syndrome characterized by the breakdown of skeletal muscle and leakage of intracellular myocyte contents, such as creatine phosphokinase (CPK) and myoglobin, into the interstitial space and plasma resulting in acute kidney injury (AKI). Elevated CPK of at least 5 times the upper limit of normal is an important diagnostic marker of Rhabdomyolysis. We present a case of rhabdomyolysis with severe AKI with a normal CPK at presentation.

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Treatment guidelines for diabetic emergencies are well described in patients with normal to moderately impaired kidney function. However, management of patients with end-stage renal disease (ESRD) is an ongoing challenge. This article describes a retrospective study comparing the rates of adverse glucose events (defined as hypoglycemia or a decrease in glucose >200 mg/dL/h) between patients with ESRD and those with normal kidney function who were admitted with diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS).

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Binding of ouabain to cardiac Na/K-ATPase initiates cell signaling and causes contractility in cardiomyocytes. It is widely accepted that caveolins, structural proteins of caveolae, have been implicated in signal transduction. It is known that caveolae play a role in Na/K-ATPase functions.

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Angiotensin II (Ang II) causes nitric oxide synthase (NOS) to become a source of superoxide (O2 (-)) via a protein kinase C (PKC)-dependent process in endothelial cells. Ang II stimulates both NO and O2 (-) production in thick ascending limbs. We hypothesized that Ang II causes O2 (-) production by NOS in thick ascending limbs via a PKC-dependent mechanism.

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Management of metabolic acidosis covers the entire spectrum from oral bicarbonate therapy and dietary modifications in chronic kidney disease to delivery of high doses of bicarbonate-based dialysate during maintenance haemodialysis (MHD). Due to the gradual depletion of the body's buffers and rapid repletion during MHD, many potential problems arise as a result of our current treatment paradigms. Several studies have given rise to conflicting data about the adverse effects of our current practice patterns in MHD.

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Adenocarcinomas and other various tumors are known to metastasize to various locations without any significant predilection and the metastasis could be the first presentation of the malignancy by the patient. Involvement of peripheral nerves without the central nervous system involvement has been rarely reported. Perineural tumor spread has been infrequently reported with soft tissue tumors without central nervous system involvement.

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Genetic dissection of the rat genome for identifying alleles that cause abnormalities in blood pressure (BP) resulted in the mapping of a significant number of BP quantitative trait loci (QTLs). In this study we mapped at least one such BP QTL on rat chromosome 10 (RNO10) as being within the introgressed segment of a S.LEW congenic strain S.

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