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Annals of Internal Medicine Nov 1945
Topics: Azotemia; Blood; Nitrogen; Typhus, Epidemic Louse-Borne
PubMed: 21003581
DOI: 10.7326/0003-4819-23-5-711 -
Journal of the American Animal Hospital... 2018Babesiosis is a hemoprotozoal tick-borne disease that is commonly associated with thrombocytopenia and anemia; however, renal involvement has been documented in dogs....
Babesiosis is a hemoprotozoal tick-borne disease that is commonly associated with thrombocytopenia and anemia; however, renal involvement has been documented in dogs. The purpose of this retrospective study was to document azotemia and proteinuria in dogs infected with Babesia sp. and to describe the response to antiprotozoal therapy. The electronic database of the North Carolina State University Vector Borne Disease Laboratory was searched to identify dogs who were diagnosed with babesiosis and to determine if they had proteinuria and/or azotemia. Dogs were excluded if they had coinfections or comorbidities known to cause glomerular injury. Of 35 dogs identified during the initial search, 5 were included; however, only 4 of these dogs had both pre- and posttreatment data. All five dogs were American pit bull terriers or American pit bull terrier-mixed breed dogs, were infected with Babesia gibsoni, and had hypoalbuminemia and proteinuria. Three dogs had azotemia. Responses to antiprotozoal treatment included normalization of (three) or increase in (one) serum albumin, resolution (one) or improvement (one) of azotemia, and reduction in proteinuria (two). Laboratory findings consistent with glomerular disease can be found in Babesia gibsoni-infected dogs, and treatment can lead to improvement of the azotemia and proteinuria.
Topics: Animals; Azotemia; Babesia; Babesiosis; DNA, Protozoan; Dog Diseases; Dogs; Proteinuria; Retrospective Studies
PubMed: 29558219
DOI: 10.5326/JAAHA-MS-6693 -
Renal Failure 2010While the fractional excretion of solutes have long been considered excellent research tools to investigate tubular physiology, their clinical use has become common over... (Review)
Review
While the fractional excretion of solutes have long been considered excellent research tools to investigate tubular physiology, their clinical use has become common over the last 40 years in the diagnoses of many disorders; however, none have reached the clinical utility of the fractional excretion of sodium in the ability to distinguish pre-renal azotemia from acute tubular necrosis. Nevertheless, there are many drugs and medical conditions that interfere with that utility and recently other solutes, including urea, uric acid and lithium, have been recently investigated to improve the diagnostic ability in clinical situations where the fractional excretion of sodium is known to be unreliable. We review the tubular physiology of these solutes and show how the differences in tubular physiology might be exploited to develop a strategy for their optimal clinical use.
Topics: Absorption; Acute Kidney Injury; Azotemia; Biological Transport, Active; Diagnosis, Differential; Humans; Kidney; Kidney Medulla; Kidney Tubules; Lithium; Nephrons; Oliguria; Sodium Chloride; Urea; Uric Acid; Water Deprivation
PubMed: 20954990
DOI: 10.3109/0886022X.2010.517353 -
Contributions To Nephrology 2007The term pre-renal azotemia (or on occasion 'pre-renal renal failure') is frequently used in textbooks and in the literature to indicate an acute syndrome characterized... (Review)
Review
The term pre-renal azotemia (or on occasion 'pre-renal renal failure') is frequently used in textbooks and in the literature to indicate an acute syndrome characterized by the presence of an increase in the blood concentration of nitrogen waste products (urea and creatinine). This syndrome is assumed to be due to loss of glomerular filtration rate but is not considered to be associated with histopathological renal injury. Thus, the term is used to differentiate 'functional' from 'structural' acute kidney injury (AKI) where structural renal injury is taken to indicate the presence of so-called acute tubular necrosis (ATN). This paradigm is well entrenched in nephrology and medicine. However, growing evidence from experimental animal models, systematic analysis of the human and experimental literature shows that this paradigm is not sustained by sufficient evidence when applied to the syndrome of septic AKI, especially in critically ill patients. In such patients, several assumptions associated with the 'pre-renal azotemia paradigm' are violated. In particular, there is no evidence that ATN is the histopathological substrate of septic AKI, there is no evidence that urine tests can discriminate 'functional' from 'structural' AKI, there is no evidence that any proposed differentiation leads or should lead to different treatments, and there is no evidence that relevant experimentation can resolve these uncertainties. Given that septic AKI of critical illness now accounts for close to 50% of cases of severe AKI in developed countries, these observations call into question the validity and usefulness of the 'pre-renal azotemia paradigm' in AKI in general.
Topics: Acute Kidney Injury; Azotemia; Critical Illness; Glomerular Filtration Rate; Humans; Kidney Glomerulus; Kidney Tubular Necrosis, Acute; Models, Biological; Prognosis; Sepsis; Syndrome
PubMed: 17464109
DOI: 10.1159/000102008 -
Critical Care Medicine Jun 2007
Topics: Acute Kidney Injury; Animals; Azotemia; Critical Illness; Kidney Function Tests; Kidney Tubules; Necrosis; Sepsis; Urinalysis
PubMed: 17522545
DOI: 10.1097/01.CCM.0000266794.57111.01 -
Tierarztliche Praxis. Ausgabe K,... Apr 2020
Topics: Acute Kidney Injury; Animals; Azotemia; Dog Diseases; Dogs; Foodborne Diseases; Fruit; Retrospective Studies; Vitis
PubMed: 32325531
DOI: 10.1055/a-1113-2361 -
The American Journal of the Medical... Dec 2020
Topics: Adult; Azotemia; Humans; Male; Renal Insufficiency; Saudi Arabia
PubMed: 32622468
DOI: 10.1016/j.amjms.2020.05.043 -
Mayo Clinic Proceedings Oct 2018
Topics: Azotemia; Humans; Kidney Function Tests; Male; Middle Aged; Skin Diseases; Sweat; Treatment Outcome; Urea; Uremia; Urinary Catheterization; Urinary Retention
PubMed: 30286839
DOI: 10.1016/j.mayocp.2018.08.026 -
Renal Failure 2008Despite proven renoprotection from RAAS blockade and its increased application since the early 1990s, we have experienced an increasing CKD/ESRD epidemic, especially... (Review)
Review
Despite proven renoprotection from RAAS blockade and its increased application since the early 1990s, we have experienced an increasing CKD/ESRD epidemic, especially among U.S. diabetics. Consequently, some concerns regarding iatrogenic azotemia from RAAS blockade have surfaced. We hypothesized that susceptible CKD patients with normal renal arteries on conventional angiography, including MRA, but who have microvascular arteriolar narrowing in the renal circulation - mimicking large vessel renal artery stenosis, even without precipitating risk factors - could experience worsening azotemia after periods of time exceeding three months on stable doses of RAAS blockade. Between September 2002 and February 2005, as part of a larger prospective study of renal failure in CKD patients on RAAS blockade, we studied five patients with >25% higher serum creatinine and normal MRA without precipitating factors. RAAS blockade was discontinued. eGFR by MDRD was monitored. Five Caucasians (M:F = 1:4; age 68 years) were enrolled and followed-up at 29.6 months. The duration of RAAS blockade at enrollment was 34.6 months. The baseline eGFR had decreased from 28.4 +/- 7.1 to 17.0 +/- 7.4 ml/min/1.73 m(2) BSA (p < 0.001) at enrollment. One required temporary hemodialysis; no deaths occurred. eGFR increased from 17.0 +/- 7.4 to 24.6 +/- 9.5 ml/min/1.73 m(2) BSA (p = 0.009), 29.6 (20-43) months after stopping the RAAS blockade. We conclude that worsening azotemia occurs in susceptible CKD patients on stable doses of RAAS blockade after long periods of time, despite normal renal arteries without precipitating risk factors. We submit that microvascular renal arteriolar narrowing is the pathophysiologic mechanism. These observations call for further study.
Topics: Adult; Aged; Aged, 80 and over; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Azotemia; Female; Glomerular Filtration Rate; Humans; Kidney; Kidney Failure, Chronic; Male; Microcirculation; Middle Aged; Renal Artery; Renin-Angiotensin System; Risk Factors
PubMed: 18197547
DOI: 10.1080/08860220701742161 -
Saudi Journal of Kidney Diseases and... May 2014Osmotic demyelination syndrome (ODS) is a dreadful, irreversible and well-recognized clinical entity that classically occurs after rapid correction of hyponatremia....
Osmotic demyelination syndrome (ODS) is a dreadful, irreversible and well-recognized clinical entity that classically occurs after rapid correction of hyponatremia. However, it has been observed that when hyponatremia is rapidly corrected in azotemic patients by hemodialysis (HD), patients do not necessarily develop ODS. We studied the effect of inadvertent rapid correction of hyponatremia with HD in patients with azotemia. Fifty-two azotemic patients, who underwent HD at the Sindh Institute of Urology and Transplantation, having pre-HD serum sodium level <125 mEq/L and post-HD serum sodium levels that increased by ≥12 mEq/L from their pre-dialysis level, were studied. Serum sodium was analyzed before and within 24 h after a HD session. HD was performed using bicarbonate solution, with the sodium concentration being 140 meq/L. The duration of the dialysis session was based on the discretion of the treating nephrologist. Patients were examined for any neurological symptoms or signs before and after HD and for up to two weeks. Magnetic resonance imaging was performed in required cases. None of the 52 patients with azotemia, despite inadvertent rapid correction of hyponatremia with HD, developed ODS. This study suggests that patients with azotemia do not develop ODS on rapid correction of hyponatremia by HD, which suggests a possible protective role of azotemia on the brain from osmotic demyelination. However, the mechanism by which azotemia protects the brain from demyelination in humans is largely hypothetical and further studies are needed to answer this question.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Azotemia; Brain; Brain Diseases; Child; Demyelinating Diseases; Female; Humans; Hyponatremia; Magnetic Resonance Imaging; Male; Middle Aged; Neurologic Examination; Osmotic Pressure; Pakistan; Renal Dialysis; Risk Factors; Syndrome; Time Factors; Treatment Outcome; Young Adult
PubMed: 24821152
DOI: 10.4103/1319-2442.132183