Lesley H. Curtis, PhD
https://medicine.duke.edu/faculty/lesley-h-curtis-phd
Lotrisone dosages: 10 mg
Lotrisone packs: 3 tubes, 4 tubes, 5 tubes, 6 tubes, 7 tubes, 8 tubes, 9 tubes, 10 tubes
Criteria for the classification of monoclonal gammopathies, multiple myeloma and related problems: a report of the International Myeloma Working Group. Impaired angiogenesis within the aging kidney: vascular endothelial progress factor and thrombospondin-1 in renal illness. Overexpression of Bcl-X(L) inhibits Ara-C-induced mitochondrial lack of cytochrome c and different perturbations that activate the molecular cascade of apoptosis. Predicting hospital mortality in critically sick cancer patients in accordance with acute kidney damage severity. Outcomes of cancer and non-cancer sufferers with acute kidney harm and need of renal alternative therapy admitted to common intensive care models. Acute renal failure secondary to solid tumor renal metastases: case report and review of the literature. Veno-occlusive illness of the liver and multiorgan failure after bone marrow transplantation: a cohort study of 355 patients. Acute renal failure with preserved renal plasma move induced by most cancers immunotherapy. Acute rhabdomyolysis as a complication of cytarabine chemotherapy for acute myeloid leukemia: case report and evaluation of literature. Renal and metabolic issues of undifferentiated and lymphoblastic lymphomas. Fenoldopam mesylate in early acute tubular necrosis: a randomized, double-blind, placebo-controlled clinical trial. Acute renal failure as a outcome of a malignant lymphoma infiltration uncovered by renal biopsy. Hematuria and decreased kidney operate as preliminary indicators of acute B-cell lymphoblastic leukemia. Tumor lysis syndrome after remedy of persistent lymphocytic leukemia with cladribine.
The potential opposed effect of this drug on renal perform has not been explored. Glomerulonephritis in liver illnesses Immunoglobulin A (IgA) nephropathy associated with liver disease is essentially the most incessantly encountered secondary type of IgA nephropathy (Newell, 1987). The pathogenesis is related to an lack of ability to remove IgA-containing complexes by Kupffer cells within the liver, which in flip predispose to deposition of IgA in the kidney. In reality, IgA deposition in the pores and skin and liver (hepatic sinusoids) make this hypothesis believable. Despite the excessive frequency of glomerular IgA deposits in superior liver disease, most sufferers are asymptomatic. Patients might present with microscopic haematuria, gentle proteinuria, and a mild degree of renal impairment. Light microscopy findings are similar to those of patients with main IgA nephropathy. Another hypothesis is related to the discharge of a putative antigen from injured hepatocytes or its manufacturing by Kupffer cells contributing to immunoglobulin formation. In addition, a decreased clearance of cryoglobulins due to liver dysfunction might lead to cryoglobulinaemia and its subsequent deposition within the kidney, pores and skin, and different tissues. The urinary 2 microglobulin was proven to be helpful in the analysis of aminoglycoside nephrotoxicity (Cabrera et al. These features have been recently confirmed in two prospective randomized managed trials evaluating terlipressin plus albumin versus albumin alone. No improvement of serum creatinine (decrease to a degree of 133 �mol/L or less) after at least 2 days of diuretic withdrawal and volume growth with albumin. The really helpful dose of albumin is 1 g/kg of physique weight per day up to a maximum of one hundred g/day. Absence of parenchymal kidney disease as indicated by proteinuria > 500 mg/day, microhaematuria (> 50 red blood cells per high power field) and/or irregular renal ultrasonography. Albumin should be given with a priming dose of 1 g/kg of physique weight adopted by 20�40 g/day. Complications associated with terlipressin remedy are related to its vasoconstrictor impact and embody ischaemic occasions in skin, tongue, fingers, intestines, and coronary heart.
Glomerular hemodynamic adjustments versus hypertrophy in experimental glomerulosclerosis. Kalra Introduction Ischaemic nephropathy is attributable to haemodynamically vital obstruction in both renal arteries, or in a single artery the place a solitary kidney is current. In 1934, Goldblatt demonstrated that unilateral renal artery stenosis may lead to bilateral renal harm by way of the event of chronic hypertension (Goldblatt, 1934). Although renal impairment ensuing from renovascular hypertension is necessary and should coexist with ischaemic nephropathy, this chapter focuses extra specifically on ischaemic renal harm occurring downstream of renal artery stenosis. Prevalence was shown to increase with age, affecting 11% of 50�56-year-olds, 18% of 60�69-year-olds, and 23% of these > 70 years of age (Coen et al. There could additionally be confounding by the high charges of coexistent diabetes and hypertension. In these with coronary artery illness, prevalence of renal artery stenosis is high, between 11% and 19. This descriptive term was first coined by Sen in 1963, though clinical descriptions date again to the nineteenth century (Sen, 1963). It has been related to Williams syndrome and neurofibromatosis, suggesting a genetic part. It may be asymptomatic or discovered after investigating options attributable to renal artery stenosis or occlusion. In the vast majority of these sufferers, hypertension is a characteristic, however the position of hypertension in contributing to renal harm is unclear (see Chapter 211). Note the irregular appearance of the normal-sized right kidney-due to hypertensive parenchymal harm. Proteinuria Proteinuria is often absent or delicate however in some sufferers could additionally be nephrotic vary. Several case research have reported significant proteinuria in the context of renal artery stenosis (Montoliu et al. In each of those case research, proteinuria was associated with excessive renin ranges and normal renal biopsy. In a subsequent case examine, administration of an angiotensin-converting enzyme inhibitor additionally led to resolution of the proteinuria with relapse on drug withdrawal (Docci et al.
Pharmacologic preconditioning effects: prostaglandin E1 induces heat-shock proteins instantly after ischemia/reperfusion of the mouse liver. Light and electron microscopic changes in proximal tubules of rats after administration of glucose, mannitol, sucrose, or dextran. Ischemia induces partial loss of floor membrane polarity and accumulation of putative calcium ionophores. Comparison of the renal hemodynamic response to unilateral and bilateral ureteral occlusion. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Macrophages use totally different internalization mechanisms to clear apoptotic and necrotic cells. Distinct pathophysiologic mechanisms of septic acute kidney harm: position of immune suppression and renal tubular cell apoptosis in murine mannequin of septic acute kidney injury. Novel roles for ceramides, calpains and caspases in kidney proximal tubule cell apoptosis: lessons from in vitro cadmium toxicity research. The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy. Aminoglycoside and glycopeptide renal toxicity in intensive care patients studied by proton magnetic resonance spectroscopy of urine. Histopathology of septic shock induced acute kidney damage: apoptosis and leukocytic infiltration. Exploration of disease mechanism in acute kidney damage utilizing a multiplex bead array assay: a nested case-control pilot examine. Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion harm in mice. Transgenic expression of proximal tubule peroxisome proliferator-activated receptor-alpha in mice confers protection throughout acute kidney damage. A role of liver fatty acid-binding protein in cisplatin-induced acute renal failure. Analysis of illness susceptibility and its relationship of pleiomorphic gene merchandise defining both immune-response genes and a restrictive requirement for cytotoxic T cells at H-2K. Targeting superoxide dismutase to renal proximal tubule cells attenuates vancomycin-induced nephrotoxicity in rats.
These vessels typically exhibit delays of several seconds and have time constants in the range of 1�2 minutes. Segmentally distinct results of depolarization on intracellular [Ca2+] in renal arterioles. Rho-kinase inhibition blunts renal vasoconstriction induced by distinct signaling pathways in vivo. Effects of dextran-induced hyperviscosity on regional blood circulate and hemodynamics in dogs. Functional proof of an inward rectifier potassium current in the renal afferent arteriole. Segment-specific differences within the inward rectifier K+ present along the renal interlobular artery. Regulation of 4-aminopyridine-sensitive, delayed rectifier K+ channels in vascular smooth muscle by phosphorylation. Effects of connexin-mimetic peptides on nitric oxide synthase- and cyclooxygenase-independent renal vasodilation. Note the extremely small dimension of afferent arteriolar myocyte in comparability with that of the mesenteric resistance artery. As described in text, smaller myocyte size may contribute to extra fast kinetics of the afferent arteriole. Image of mesenteric artery myocyte was provided by Dr Francis Plane, University of Alberta. Regulation of calcium-activated chloride channels in easy muscle cells: a fancy picture is emerging. Murine vasa recta pericyte chloride conductance is controlled by calcium, depolarization, and kinase activity. Atrial natriuretic peptide causes pre-glomerular vasodilatation and post-glomerular vasoconstriction in rat kidney. Vessel- and vasoconstrictor-dependent position of rho/rho-kinase in renal microvascular tone.
This figure will increase to nearly 20 times in patients undergoing emergency procedures (Bailes, 2000). The mean age of the sufferers was 63 years, with 25% aged > 75 years (Joannidis et al. Renal hypoperfusion can develop in several clinical situations, similar to reduced cardiac output (myocardial dysfunction and pericardial disease), inside quantity distribution to interstitial spaces (cirrhosis, nephrotic syndrome, sepsis, and malnutrition), and exterior loss of fluids with insufficient fluid alternative (vomiting, diarrhoea, bleeding, and extreme sweating because of febrile illnesses). Dehydration and volume depletion occur frequently in the aged, affecting almost 1% of hospital admissions in this inhabitants (Lavizzo-Mourey et al. Being bedridden and having poor fluid oral consumption are important risk factors for dehydration, usually related to significant hypernatremia which, if untreated, has a very excessive mortality fee (Weinberg et al. They are usually associated with atherosclerosis, atrial fibrillation, or myocardial infarction. Moreover, older patients appear to have the next incidence of antineutrophil cytoplasmic antibody and antiglomerular basement membrane-associated quickly progressive glomerulonephritis (Preston et al. Finally, older sufferers are prone to creating rhabdomyolysis within the setting of acute immobilization, infectious diseases, cerebrovascular accidents, hyperosmolar state, hyponatraemia, hypernatraemia, hypothermia, and after falls. The obstruction could also be both intrinsic or extrinsic and might happen at any stage of the urinary tract. Among the causes of lower urinary tract obstruction, the most common in males is prostatic enlargement because of benign prostatic hypertrophy or carcinoma. Benign prostatic hypertrophy is the most typical neoplasm in males, affecting 50% of males aged 50 years and increasing to 90% by the ninth decade of life. The second commonest cause in males is urethral stricture disease, often secondary to trauma. Moreover, dehydration and volume depletion circumstances may be worsened by the concomitant administration of diuretics, laxatives, and medicines that lower urge for food or the level of consciousness. Aminoglycosides have a direct toxic impact on the epithelial tubular cells, while ciclosporin is answerable for a lower in renal perfusion. The dose of the drug administered and the duration of the therapy are determinant components for possible regression of the kidney injury. Proton pump inhibitors, often secure and regularly prescribed in the aged, have been related to acute interstitial nephritis as well (Ni et al.
Hyperoxaluria in idiopathic calcium stone disease: further evidence of intestinal hyperabsorption of oxalate. The hypocalciuric or benign variant of familial hypercalcemia: scientific and biochemical features in fifteen kindreds. Divalent cation metabolism: famalial hypocalciuric hypercalcemia veersus typical major hyperparathyroidism. Pathogenesis and scientific course of mixed calcium oxalate and uric acid nephrolithiasis. A lack of distinctive pathophysiologic background for nephrolithiasis of major hyperparathyroidism. Correction of hypocitraturia and prevention of stone formation by combined thiazide and potassium citrate remedy in thiazide-unresponsive hypercalciuric nephrolithiasis. Urine stone threat components in nephrolithiasis sufferers with and with out bowel disease. Biochemical method to prognosis and differentiation of main hyperoxalurias: an update. Incomplete renal tubular acidosis and bone mineral density: a population survey in an area of endemic renal tubular acidosis. Stone disease within the Hmong of Minnesota: preliminary description of a high-risk population. Plasma oxalate concentration and oxalate distribution volume in sufferers with normal and decreased renal operate. Effect of potassium magnesium citrate on thiazide-induced hypokalemia and magnesium loss. The effect of crystalline monosodium urate on the crystallization of calcium oxalate in entire human urine. Secondary distal renal tubular acidosis in affiliation with urological abnormalities.
Serum cystatin C concentrations are apparently impartial of body mass, gender, infections, and malignancies, however confounding has been reported for thyroid ailments, spina bifida, diabetic ketoacidosis, and generalized inflammation (Zaffanello et al. Concentrations are larger in preterm than at-term infants and decline in the course of the first month of life. So far, a number of of these candidates have proven usefulness in medical studies (see additionally Chapter 223). Also, it ought to be emphasized that medical validation research have most commonly been performed in single centres within the post-cardiac surgical procedure setting, the place the renal insult happens at a definite time level and the investigated patient cohort is relatively homogeneous. It is freely filtered by the glomerulus and virtually utterly reabsorbed at the proximal tubule, thus elevated urinary excretion suggests proximal tubule harm (Mishra et al. The affiliation was lost when adjusting for fluid stability, suggesting that the protective impact of furosemide was associated to the optimization of fluid control (Grams et al. Once these hurdles are overcome, a subsequent, even more difficult step in path of providing therapeutic profit from biomarker research will be to Theophylline Theophylline, a xanthine spinoff with non-specific adenosine receptor antagonistic properties, was proven experimentally to reverse renal vasoconstriction throughout hypoxic episodes in rabbits (Gouyon and Guignard, 1988). In 4 independent trials in neonates with extreme perinatal asphyxia, a single low-dose theophylline bolus (5�8 mg/kg) administered throughout the first hour of life led to a significantly higher estimated creatinine clearance (22 vs 6. Comparable results were reported for preterm neonates receiving theophylline for respiratory distress syndrome (1 mg/ kg/day for three consecutive days) (Cattarelli et al. Dopamine Dopamine binds to peripheral dopamine (D1/D2), alpha- and beta-adrenergic receptors. Dopamine at low dosage dilates the interlobular arteries and glomerular arterioles in rats, whereas greater doses reduce renal blood move through alpha-adrenergic effects (Steinhausen et al. In sick preterm neonates, dopamine (6 micrograms/kg/min) increases renal blood move and urine output (Seri et al. Fenoldopam Fenoldopam (a selective dopamine D1 receptor and average 2-adrenoreceptor agonist) dose-dependently will increase renal blood move and reduces systemic blood strain in canines (Hahn et al. The critical degree of initial fluid overload associated with increased mortality appeared to be a rise in physique weight by 10�15%. Of observe, a recent large-scale randomized medical trial of fluid bolus therapy in African kids with severe dehydration because of infections revealed a 45% enhance in mortality associated with the usage of aggressive (20�45 mL/kg) saline or albumin fluid boluses (Maitland et al.
Keldron, 36 years: Analysis of magnesium and hint parts in urinary calculi by atomic absorption spectrophotometry.
Diego, 26 years: Europe, United States, and Australia) an infection normally occurs during adolescence or maturity (either parenterally or by way of sexual contact).
Onatas, 43 years: In chronic bacterial prostatitis, antibiotics ought to be trialled at excessive dose for 2 weeks in the first occasion.
Peer, 33 years: Ionic and non-ionic hyperosmolar radiocontrast media, first and second generations of iodine-containing contrast agents, together with dehydration, are well-known causes of osmotic nephrosis.
Arokkh, 46 years: Indian studies have recommended initial administration of 20�100 mL, adopted by repeat dosage of 25�50 mL each 4�6 hours until the effects of systemic envenoming disappear.
Amul, 55 years: As the liquid is pumped out of the field and thru the dialyser, urea is removed or cleared from the liquid which is then returned to the field.
Roland, 34 years: Rapid saline infusion produces hyperchloremic acidosis in sufferers undergoing gynecologic surgical procedure.
Daro, 21 years: Calcineurin inhibitors Ciclosporin and tacrolimus are essential drugs used to prevent the rejection of transplanted organs.
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