Although combined cardiac and renal dysfunction is common in hospitalized patients and portends a poor prognosis, lack of understanding of the pathogenesis and classification of the condition has hampered the development of therapeutic strategies. Interactions between the heart and kidney involve multiple hemodynamic and nonhemodynamic factors and are usually bidirectional, as acute or chronic dysfunction of the cardiac or renal systems can negatively affect one another. This review introduces a new definition and classification system of cardiorenal syndrome advocated by a consensus conference of the Acute Dialysis Quality Initiative and summarizes the current understanding of cardiorenal syndrome.
Acute Kidney Injury ; Cardio-Renal Syndrome* ; Cardiovascular Diseases ; Classification ; Consensus ; Dialysis ; Heart ; Heart Failure ; Hemodynamics ; Humans ; Kidney ; Prognosis ; Renal Insufficiency, Chronic

To maintain homeostasis of the cardiovascular system, the heart and kidney act bidirectionally. Therefore, acute or chronic dysfunction of one organ can cause dysfunction in the other. This phenomenon is characterized as cardiorenal syndrome (CRS). Concurrent dysfunction of the heart and kidney adversely affects one another and eventually worsens patient outcomes through a vicious cycle. Although a CRS classification system has been proposed, the underlying pathophysiology is multifactorial and clinical access continues to be difficult. Although several therapies, including agents that target the renin-angiotensin-aldosterone system, have been utilized, there is not enough evidence to demonstrate their effectiveness for CRS. Thus, more effort should be made to optimize the diagnosis and treatment strategies for CRS patients. This review will introduce CRS as it is currently understood, discuss the pathophysiology, and examine management strategies.
Acute Kidney Injury ; Cardio-Renal Syndrome ; Cardiovascular System ; Classification ; Diagnosis ; Heart ; Heart Failure ; Homeostasis ; Humans ; Kidney ; Renal Insufficiency, Chronic ; Renin-Angiotensin System

Hemodialysis using Kiil type artificial kidney was performed on two cases of acute renal failure and a case of chronic renal failure and the following results were obtained: 1. A case of acute renal failure recovered from her deteriorated renal function following four consecutive hemodialyses and another following a single hemodialysis of six hours. 2. A case of chronic renal failure is now stabilized clinically and maintained on ambulatory intermittent long-term hemodialysis.
Acute Kidney Injury ; Kidney Failure, Chronic ; Kidneys, Artificial* ; Renal Dialysis* ; Renal Insufficiency*

Renal failure due to nephrocalcinosis after large-bowel cleansing with sodium phosphate preparations before endoscopic procedures is an easily overlooked diagnosis. While it has been reported that acute renal failure can result from the use of oral sodium phosphate preparations, chronic renal failure has not yet been reported. We report a case of chronic renal failure due to oral sodium phosphate, in which a kidney biopsy was performed.
Acute Kidney Injury ; Biopsy ; Cathartics ; Kidney ; Kidney Failure, Chronic ; Nephrocalcinosis ; Phosphates ; Renal Insufficiency ; Sodium

No abstract available.
Humans ; Hypertension* ; Kidney Failure, Chronic* ; Renal Insufficiency*

No abstract available.
Humans ; Hypertension* ; Kidney Failure, Chronic* ; Renal Insufficiency*

No abstract available.
Child* ; Humans ; Kidney Failure, Chronic* ; Renal Insufficiency*

BACKGROUND: Preoperative elevated serum creatinine values are associated with increased risk for both morbidity and mortality in patients undergoing on-pump coronary artery bypass surgery (CABG). We investigated the postoperative changes of renal function and proper management in the patients. MATERIAL AND METHOD: Among 74 consecutive patients who underwent isolated on-pump CABG, 17 patients with increased serum creatinine level (creatinine > or = 1.5 mg/dL) within preoperative one week were included in the study. Seven patients showed preoperative serum creatinine level of 2.0 mg/dL or higher, and 3 of them had been undergoing hemodialysis. Preoperative hemodialysis was performed in the 3 patients due to end-stage renal failure (ESRD) the day before the operation. We started peritoneal dialysis immediately after the cardiopulmonary bypass in patients with ESRD or postoperative acute renal failure if it was necessary to remove intravascular volume and lower serum creatinine level. RESULT: In most of the patients with CABG, postoperative serum creatinine level increased and recovered to the preoperative level at the discharge. In 2 of the 4 patients with serum creatinine level of 2.0 mg/dL or higher and 3 patients with ESRD, intravascular volume, serum creatinine level and serum electrolyte were controlled with peritoneal dialysis. CONCLUSION: Postoperative serum creatinine level increased transiently in most of CABG patients, and intravascular volume and serum creatinine level were controlled by peritoneal dialysis only in the patients with acute renal failure postoperatively and those depending on hemodialysis.
Acute Kidney Injury ; Cardiopulmonary Bypass ; Coronary Artery Bypass ; Creatinine* ; Humans ; Kidney Failure, Chronic ; Mortality ; Peritoneal Dialysis ; Renal Dialysis ; Renal Insufficiency

Although it was thought that survivors from an acute kidney injury (AKI) recovered kidney function completely, cumulative observational data have shown that AKI can cause end-stage renal disease directly, increase the risk of developing incident chronic kidney disease (CKD), and worsen an underlying CKD. These data have confirmed an association between AKI and an increased risk of permanent kidney damage, with subsequent development of CKD. However, many studies have focused on early injury following ischemic insult; the mechanisms of long-term injury remain poorly understood. Established and new data suggest that endothelial injury, loss of peritubular capillary volume, and chronic hypoxia affect structural changes after an ischemic insult. The repair process after acute kidney injury can be both adaptive and maladaptive. A maladaptive response includes persistent upregulation of proinflammatory and profibrotic signals and maladaptive cellular regeneration; this is thought to be one of the mechanisms leading to progressive renal injury and, ultimately, end-stage renal disease. The purpose of this brief review was to focus on recent advances related to the mechanisms of the progression from AKI to CKD. This review suggests that a new approach is required to manage AKI patients to prevent and/or arrest CKD progression.
Acute Kidney Injury* ; Anoxia ; Capillaries ; Humans ; Inflammation ; Kidney ; Kidney Failure, Chronic ; Regeneration ; Renal Insufficiency, Chronic* ; Survivors ; Up-Regulation

Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal, inducible, and endothelial NOS (n/i/eNOS). NO-mediated effects can be beneficial or harmful depending on the specific risk factors affecting the disease. In hypertension, the vascular relaxation response to acetylcholine is blunted, and that to direct NO donors is maintained. A reduction in the activity of eNOS is mainly responsible for the elevation of blood pressure, and an abnormal expression of iNOS is likely to be related to the progression of vascular dysfunction. While eNOS/nNOS-derived NO is protective against the development of atherosclerosis, iNOS-derived NO may be proatherogenic. eNOS-derived NO may prevent the progression of myocardial infarction. Myocardial ischemia/reperfusion injury is significantly enhanced in eNOS-deficient animals. An important component of heart failure is the loss of coronary vascular eNOS activity. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2 abundance. In chronic kidney disease model of subtotal-nephrectomized rats, treatment with NOS inhibitors decreased systemic NO production and induced left ventricular systolic dysfunction (renocardiac syndrome).
Acetylcholine ; Animals ; Aquaporin 2 ; Atherosclerosis ; Blood Pressure ; Cardio-Renal Syndrome ; Diabetes Insipidus, Nephrogenic ; Fibrosis ; Heart Failure ; Humans ; Hypertension ; Hypertrophy, Left Ventricular ; Kidney ; Mice ; Myocardial Infarction ; Myocardium ; Neurons ; Nitric Oxide ; Rats ; Relaxation ; Renal Insufficiency, Chronic ; Risk Factors ; Tissue Donors ; Ureteral Obstruction