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The authors investigated whether tolvaptan, an orally active vasopressin V 2 -receptor antagonist that promotes electrolyte-free water loss, might improve hyponatremia. Serum sodium concentrations in patients with euvolemic or hypervolemic hyponatremia and mild or marked hyponatremia improved with therapy at day 4 and day 30. Tolvaptan holds promise for treating patients with hyponatremic states. Serum sodium concentrations in patients with euvolemic or hypervolemic hyponatremia and mild or marked hyponatremia improved with tolvaptan therapy. Tolvaptan holds promise for treating patients with hyponatremic states. Hyponatremia, the most common electrolyte derangement occurring in hospitalized patients, 1 , 2 is usually classified as hypovolemic, euvolemic, or hypervolemic. The secretion of arginine vasopressin appears to be of central importance in the decline of serum sodium concentrations in all these conditions. 1 , 2 Hyponatremia is reported to be associated with increased morbidity and mortality among patients with heart, liver, or neurologic disease. 3 – 8 Even mild chronic hyponatremia has been associated with subtle neurologic defects, manifested as impairments in balance and attention that can increase the incidence of falls. 9 These deficits may be reversed with the correction of the hyponatremia. Tolvaptan, a . . .

Renal failure, a challenging complication of cirrhosis, is one of the most important risk factors for liver transplantation. In recent years, substantial progress has been made toward understanding the pathogenesis and natural history of renal failure in cirrhosis. This review discusses recently identified information about renal failure in cirrhosis and clinical interventions that may assist in the prevention and management of this complication. Substantial progress has been made toward understanding the pathogenesis and natural history of renal failure in cirrhosis. This review discusses recently identified information about renal failure in cirrhosis and clinical interventions that may assist in the prevention and management of this complication. Renal failure is a challenging complication of cirrhosis 1 , 2 and is one of the most important risk factors when liver transplantation is being considered. Patients with cirrhosis and renal failure are at high risk for death while awaiting transplantation and have an increased frequency of complications and reduced survival after transplantation, as compared with those without renal failure. 3 , 4 In 2002, the Model for End-Stage Liver Disease (MELD) score — derived from measurements of serum bilirubin, the international normalized ratio of prothrombin time, and serum creatinine to evaluate pretransplantation renal function — was introduced as an aid to organ allocation . . .

Effects of aggressive blood pressure control in normotensive type 2 diabetic patients on albuminuria, retinopathy and strokes. Although several important studies have been performed in hypertensive type 2 diabetic patients, it is not known whether lowering blood pressure in normotensive (BP <140/90mm Hg) patients offers any beneficial results on vascular complications. The current study evaluated the effect of intensive versus moderate diastolic blood pressure (DBP) control on diabetic vascular complications in 480 normotensive type 2 diabetic patients. The current study was a prospective, randomized controlled trial in normotensive type 2 diabetic subjects. The subjects were randomized to intensive (10mm Hg below the baseline DBP) versus moderate (80 to 89mm Hg) DBP control. Patients in the moderate therapy group were given placebo, while the patients randomized to intensive therapy received either nisoldipine or enalapril in a blinded manner as the initial antihypertensive medication. The primary end point evaluated was the change in creatinine clearance with the secondary endpoints consisting of change in urinary albumin excretion, progression of retinopathy and neuropathy and the incidence of cardiovascular disease. The mean follow-up was 5.3 years. Mean BP in the intensive group was 128 ± 0.8/75 ± 0.3mm Hg versus 137 ± 0.7/81 ± 0.3mm Hg in the moderate group, P < 0.0001. Although no difference was demonstrated in creatinine clearance (P = 0.43), a lower percentage of patients in the intensive group progressed from normoalbuminuria to microalbuminuria (P = 0.012) and microalbuminuria to overt albuminuria (P = 0.028). The intensive BP control group also demonstrated less progression of diabetic retinopathy (P = 0.019) and a lower incidence of strokes (P = 0.03). The results were the same whether enalapril or nisoldipine was used as the initial antihypertensive agent. Over a five-year follow-up period, intensive (∼128/75mm Hg) BP control in normotensive type 2 diabetic patients: (1) slowed the progression to incipient and overt diabetic nephropathy; (2) decreased the progression of diabetic retinopathy; and (3) diminished the incidence of stroke.

Diuretics play significant role in pharmacology and treatment options in medicine. This paper aims to review and evaluate the clinical use of diuretics in conditions that lead to fluid overload in the body such as cardiac failure, cirrhosis, and nephrotic syndrome. To know the principles of treatment it is essential to understand the underlying pathophysiological mechanisms that cause the need of diuresis in the human body. Various classes of diuretics exist, each having a unique mode of action. A systemic approach for management is recommended based on the current guidelines, starting from thiazides and proceeding to loop diuretics. The first condition for discussion in the paper is cardiac failure. Treatment of ascites in liver cirrhosis with spironolactone as the primary agent is highlighted with further therapeutic options. Lastly, management choices for nephrotic syndrome are discussed and recommended beginning from basic sodium restriction to combined diuretic therapies. Major side effects are discussed.

Although in some parts of the world acute and chronic kidney diseases are preventable or treatable disorders, in many other regions these diseases are left without any care. The nephrology community needs to commit itself to reduction of this divide between high-income and low-income regions. Moreover, new and exciting developments in fields such as pharmacology, genetic, or bioengineering, can give a boost, in the next decade, to a new era of diagnosis and treatment of kidney diseases, which should be made available to more patients.

Glomerular hyperfiltration occurs as a physiological response during pregnancy and after consumption of high-protein meals, but an elevation in glomerular filtration rate is also associated with various disease states. In this Review, the authors discuss the definitions of glomerular hyperfiltration as well as the underlying mechanisms and hemodynamic changes that can adversely affect kidney function. They also describe potential approaches to treat glomerular hyperfiltration. Glomerular hyperfiltration is a phenomenon that can occur in various clinical conditions including kidney disease. No single definition of glomerular hyperfiltration has been agreed upon, and the pathophysiological mechanisms, which are likely to vary with the underlying disease, are not well explored. Glomerular hyperfiltration can be caused by afferent arteriolar vasodilation as seen in patients with diabetes or after a high-protein meal, and/or by efferent arteriolar vasoconstriction owing to activation of the renin–angiotensin–aldosterone system, thus leading to glomerular hypertension. Glomerular hypertrophy and increased glomerular pressure might be both a cause and a consequence of renal injury; understanding the renal adaptations to injury is therefore important to prevent further damage. In this Review, we discuss the current concepts of glomerular hyperfiltration and the renal hemodynamic changes associated with this condition. A physiological state of glomerular hyperfiltration occurs during pregnancy and after consumption of high-protein meals. The various diseases that have been associated with glomerular hyperfiltration, either per nephron or per total kidney, include diabetes mellitus, polycystic kidney disease, secondary focal segmental glomerulosclerosis caused by a reduction in renal mass, sickle cell anemia, high altitude renal syndrome and obesity. A better understanding of the mechanisms involved in glomerular hyperfiltration could enable the development of new strategies to prevent progression of kidney disease. Key Points Glomerular hyperfiltration has been variably defined either as an abnormally high whole-kidney glomerular filtration rate (GFR), increased filtration fraction, or as increased filtration per nephron An increased GFR occurs physiologically after consuming a high-protein meal and during pregnancy Increased GFR can occur as an early manifestation of disease, for example in diabetes mellitus, but it remains to be proven whether glomerular hyperfiltration is a precursor of chronic kidney disease Increased filtration per nephron occurs as an adaptive response to nephron loss, and leads to glomerular hypertension and subsequent glomerulosclerosis with progressive renal function decline The mechanisms of glomerular hyperfiltration in disease conditions are variable and not entirely clear, although the renin–angiotensin–aldosterone system has been implicated as a contributing pathway Longitudinal studies are needed to examine whether treatment of glomerular hyperfiltration will slow the progression of chronic kidney disease; this research requires uniform, pathophysiologically based definitions of glomerular hyperfiltration

Acute tubular necrosis (ATN) is common in hospitalized patients, particularly in the intensive care unit. Over the past four decades, the mortality rate from ATN has remained at 50% to 80%. To review recent studies of diagnosis and treatment strategies for ATN. MEDLINE search for all clinical studies of therapies for ATN, supplemented by a review of the references of the identified articles. Prospective studies and major retrospective studies evaluating therapies for ATN. Data on the study sample, interventions performed, results, side effects, and duration of follow-up. Early diagnosis of ATN by exclusion of prerenal and postrenal causes of acute renal failure, examination of urinary sediment, and analysis of urine measures (for example, fractional excretion of sodium in the absence of diuretics) can allow the early involvement of nephrologists and improve survival. Enteral rather than parenteral hyperalimentation in severely malnourished patients may improve survival. Sepsis causes 30% to 70% of deaths in patients with ATN; therefore, avoidance of intravenous lines, bladder catheters, and respirators is recommended. Because septic patients are vasodilated, large volumes of administered fluid accumulate in the lung interstitium of these patients. This condition necessitates ventilatory support, which when prolonged leads to acute respiratory distress syndrome, multiorgan failure, and increased mortality. More aggressive dialysis (for example, given daily) with biocompatible membranes may improve survival in some patients with acute renal failure. New information about the importance of early diagnosis and supportive care for patients with ATN has emerged. However, randomized trials of these interventions are needed to test their effect on the morbidity and mortality of ATN.

The combination of acute renal failure and sepsis is associated with an ominous 70 percent mortality. This article discusses the substantial progress in understanding the mechanisms of sepsis-associated acute renal failure. Interventions based on pathogenetic factors may reduce both incidence and mortality. Acute renal failure occurs in approximately 19 percent of patients with moderate sepsis, 23 percent with severe sepsis, and 51 percent with septic shock when blood cultures are positive (Table 1 and Table 2). 1 , 2 A progressive increase in the acute respiratory distress syndrome also occurs with moderate and severe sepsis and septic shock. In the United States, an estimated 700,000 cases of sepsis occur each year, resulting in more than 210,000 deaths; this number accounts for 10 percent of all deaths annually and exceeds the number of deaths due to myocardial infarction. 3 The combination of acute renal failure and sepsis is . . .

This Review describes the cardiovascular manifestations of autosomal-dominant polycystic kidney disease (ADPKD), including hypertension, left ventricular hypertrophy, aneurysms and cardiac valvular disorders. The authors focus particularly on hypertension, with a detailed discussion of the pathogenesis of this condition in ADPKD and a comprehensive review of the renal and cardiovascular effects of antihypertensive treatment in the ADPKD setting. Recommendations for the optimal cardiovascular management of ADPKD are provided. Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal-dominant polycystic kidney disease (ADPKD). Hypertension is a common early symptom of ADPKD, and occurs in approximately 60% of patients before renal function has become impaired. Hypertension is associated with an increased rate of progression to end-stage renal disease and is the most important potentially treatable variable in ADPKD. Left ventricular hypertrophy, which is a powerful, independent risk factor for cardiovascular morbidity and mortality, also occurs frequently in patients with ADPKD. Both hypertension and left ventricular hypertrophy have important roles in cardiovascular complications in these individuals. Moreover, biventricular diastolic dysfunction, endothelial dysfunction, increased carotid intima–media thickness, and impaired coronary flow velocity reserve are present even in young patients with ADPKD who have normal blood pressure and well-preserved renal function. These findings suggest that cardiovascular involvement starts very early in the course of ADPKD. Intracranial and extracranial aneurysms and cardiac valvular defects are other potential cardiovascular problems in patients with ADPKD. Early diagnosis and treatment of hypertension, with drugs that block the renin–angiotensin–aldosterone system, has the potential to decrease the cardiovascular complications and slow the progression of renal disease in ADPKD. Key Points Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal-dominant polycystic kidney disease (ADPKD) Hypertension, a common symptom of ADPKD, is associated with rapid progression to end-stage renal disease; the renin–angiotensin–aldosterone system (RAAS) is important in the development of hypertension in this setting Early vascular changes have been reported even in young patients with ADPKD and normal blood pressure Left ventricular hypertrophy is a common finding in patients with ADPKD Patients with ADPKD have a higher prevalence of aneurysms and cardiac valvular abnormalities than the general population Early and effective treatment of hypertension is very important to decrease the morbidity and mortality of patients with ADPKD, and drugs that inhibit the RAAS might be beneficial in this context

Acute renal failure (ARF), characterized by sudden loss of the ability of the kidneys to excrete wastes, concentrate urine, conserve electrolytes, and maintain fluid balance, is a frequent clinical problem, particularly in the intensive care unit, where it is associated with a mortality of between 50% and 80%. In this review, the epidemiology and pathophysiology of ARF are discussed, including the vascular, tubular, and inflammatory perturbations. The clinical evaluation of ARF and implications for potential future therapies to decrease the high mortality are described.