scholarly journals Renal failure in patients with hematological malignancies (literature review)

2021 ◽  
Vol 16 (4) ◽  
pp. 59-63
Author(s):  
E. G. Gromova
Keyword(s):  
Renal Failure ◽  
Organ Failure ◽  
Renal Injury ◽  
Hematological Malignancies ◽  
Tumor Lysis Syndrome ◽  
Individual Characteristics ◽  
Toxic Effects ◽  
Acute Renal Injury ◽  
Antitumor Therapy ◽  
Anticancer Treatment

Dysfunction of the natural detoxification organs remains a significant problem in patients with hematological malignancies. The reasons for the development of renal failure are associated with the individual characteristics of the malignant process, the patient’s comorbid background, the toxic effects of anticancer treatment and its complications. The efficacy of many anticancer drugs correlates with their dose, an increase in which is associated with increased toxic effects on healthy organs, including the kidneys. The main reasons for the renal failure development in hematological cancer patients and syndromes that prevent adequate antitumor therapy are considered. Diagnostic algorithm optimization and supportive intensive care of acute renal failure is the key to the successful application of highly effective modern protocols of drug anticancer treatment.A special group is represented by patients suffering from monoclonal gammopathies with acute renal injury and hyperproduction of immunoglobulins free light chains. Renal failure can be the onset and dominant clinical manifestation of multiple myeloma in 18–56 % of cases, of which 10 % require programmed hemodialysis. Antitumor therapy in presence of renal failure is limited, and in some cases impossible, while the renal function recovery is associated with an increase in survival.Organ damage in oncohematological patients can be a manifestation of paraneoplastic syndromes. Tumor lysis syndrome is an urgent problem of oncohematological practice associated with the development of acute renal injury and high mortality.The development of organ failure in oncohematological patients causes significant difficulties in antitumor therapy; a combination of organ dysfunction and the resulting change in anticancer therapy regimens worsen the prognosis. Modern methods of organ failure prevention and treatment can successfully solve complex clinical problems.

scholarly journals Incidence of Acute Renal Failure in Full Term Neonates with Birth Asphyxia

2019 ◽  
Vol 4 (1) ◽  
pp. 671-674
Author(s):  
Chandra Bhushan Jha ◽  
Akhil Tamrakar
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Injury ◽  
Urine Output ◽  
Birth Asphyxia ◽  
Full Term ◽  
Acute Renal Injury ◽  
Term Neonates ◽  
Oliguric Renal Failure

Introduction: Birth asphyxia is an eventuality having far reaching consequences in the neonatal period. Hypoxia and ischemia can cause damage to almost every tissue and organ in the body and various target organs involved. Renal insult is a recognized complication of birth asphyxia and carries a poor prognosis. Timely detection of renal dysfunction and appropriate management may favorably alter the prognosis in many neonates with birth asphyxia. Objective: The present study was done to find out the incidence of acute renal failure in the full term neonates with birth asphyxia. Methodology: A cross sectional study was conducted at Birat Medical College Teaching Hospital, Morang, Nepal from 1st September 2017 to 28th February 2018. Fifty full term neonates born with Apgar score of <6 at 5 minutes and fulfilling inclusion criteria were enrolled in the study. Asphyxiated neonates having Serum creatinine >1.5gm/dl or urine output<1ml/kg/hr were labeled as cases of Acute Renal Failure. Blood sample for serum creatinine was collected at 24hrs, 48 hrs and 72 hrs of life. Results A total of 50 term asphyxiated neonates were enrolled in the present study. Among them 54% and 46% were males and females respectively with male to female ratio of 1.2:1. In the present study 62% of cases developed acute renal failure in either of the first three days of life with mean urine output 1.02±0.27ml/kg/hr and mean serum creatinine of 1.49±0.32 mg/dL. The incidence of oliguric renal failure was 52% and non oliguric renal failure was 48%.The association between serum creatinine and urine output was statistically significant. Conclusion: In the present study birth asphyxia has been an important cause of neonatal acute renal injury, revealing 31 (62%) cases. Monitoring urine output and serum creatinine has helped in detecting the asphyxiated neonates with acute renal injury in the early stage.

Renal Insufficiency and Failure

Hematology ◽  
2010 ◽  
Vol 2010 (1) ◽  
pp. 431-436 ◽  
Author(s):  
Meletios A. Dimopoulos ◽  
Evangelos Terpos
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Renal Impairment ◽  
Renal Disease ◽  
Renal Injury ◽  
Filtration Rate ◽  
Acute Renal Injury ◽  
Sustained Improvement ◽  
Definition Of

Abstract Renal impairment is a common complication of multiple myeloma. Chronic renal failure is classified according to glomerular filtration rate as estimated by the MDRD (modification of diet in renal disease) formula, while RIFLE (risk, injury, failure, loss and end-stage renal disease) and AKIN (acute renal injury network) criteria may be used for the definition of the severity of acute renal injury. Novel criteria based on estimated glomerular filtration rate measurements are proposed for the definition of the reversibility of renal impairment. Renal complete response (CRrenal) is defined as sustained (i.e., lasting at least 2 months) improvement of creatinine clearance (CRCL) from under 50 mL/min at baseline to 60 mL/min or above. Renal partial response (PRrenal) is defined as sustained improvement of CRCL from under 15 mL/min at baseline to 30 to 59 mL/min. Renal minor response (MRrenal) is defined as sustained improvement of the baseline CRCL of under 15 mL/min to 15 to 29 mL/min or, if baseline CRCL was 15 to 29 mL/min, improvement to 30 to 59 mL/min. Bortezomib with high-dose dexamethasone is considered the treatment of choice for myeloma patients with renal impairment and improves renal function in most patients. Although there is limited experience with thalidomide, this agent can be administered at the standard dosage to patients with renal failure. Lenalidomide, when administered at reduced doses according to renal function, is effective and can reverse renal impairment in a subset of myeloma patients.

BIOMARKERS OF ACUTE RENAL INJURY AND RENAL FAILURE

Shock ◽  
2006 ◽  
Vol 26 (3) ◽  
pp. 245-253 ◽  
Author(s):  
Ronald J. Trof ◽  
Francesco Di Maggio ◽  
Jan Leemreis ◽  
A.B. Johan Groeneveld
Keyword(s):  
Renal Failure ◽  
Renal Injury ◽  
Acute Renal Injury

Prognostic significance of acute renal injury in acute tumor lysis syndrome

2009 ◽  
Vol 51 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Michael Darmon ◽  
Isabelle Guichard ◽  
François Vincent ◽  
Benoit Schlemmer ◽  
Élie Azoulay
Keyword(s):  
Renal Injury ◽  
Tumor Lysis Syndrome ◽  
Prognostic Significance ◽  
Acute Renal Injury ◽  
Tumor Lysis

scholarly journals PROLONGED PYREXIA WITH ACUTE RENAL INSULT - UNRAVELING THE PUZZLE AND SOLVING THE ENIGMA

2014 ◽  
Vol 04 (02) ◽  
pp. 129-132
Author(s):  
Raghava Sharma
Keyword(s):  
Renal Failure ◽  
Renal Injury ◽  
Peripheral Blood ◽  
Fever Of Unknown Origin ◽  
Unknown Origin ◽  
Acute Renal Injury ◽  
Middle Aged ◽  
Blood Eosinophilia ◽  
Oliguric Renal Failure ◽  
Peripheral Blood Eosinophilia

Abstract:A middle aged man with prolonged pyrexia was referred to us with a diagnosis of FUO (Fever of unknown origin). He was evaluated by various investigations and a diagnosis of Tuberculosis was established. On anti tubercular treatment (ATT) he developed complication of acute renal injury –non oliguric renal failure, from which he recovered fully after the puzzle was successfully solved & managed accordingly. Even though he was proved to have rifampicin induced acute intersticial nephritis(AIN) by biopsy , he had varied & unconventional presentation like without oliguria, without peripheral blood eosinophilia, and more so particularly on the maiden administration of rifampicin. Thus our case highlights the importance of quickly establishing the cause for FUO, and also need for greater vigilance on part of physicians to solve unconventional presentations of complications arising out of treatment.

scholarly journals Therapeutic use of growth factors in renal failure.

1994 ◽  
Vol 5 (1) ◽  
pp. 1-11
Author(s):  
M R Hammerman ◽  
S B Miller
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factors ◽  
Chronic Renal Failure ◽  
Growth Factor ◽  
Renal Injury ◽  
Kidney Development ◽  
Therapeutic Agents ◽  
Acute Renal Injury ◽  
Igf I

Polypeptide growth factors regulate kidney development, growth, and function and participate in processes of repair after renal injury. The use of one or more growth factors as therapeutic agents has been proposed in the settings of acute and chronic renal failure. In animal models of acute renal injury, the administration of epidermal growth factor, insulin-like growth factor I (IGF-I), or hepatocyte growth factor accelerates the restoration of kidney function and the normalization of histology post-acute renal injury and reduces mortality. The mechanisms by which the growth factors act in acute renal failure include the stimulation of anabolism, the maintenance of glomerular filtration, and the enhancement of tubular regeneration. IGF-I has been safely administered to humans with chronic renal failure. The growth factor enhances GFR and RPF in these individuals. Further studies will be required to establish a role for IGF-I or other growth factors as therapeutic agents for acute renal failure in humans and to define the utility of IGF-I as a medical therapy for chronic renal insufficiency.

scholarly journals Prolonged renal failure in the course of atypical ethylene glycol intoxication.

2013 ◽  
Vol 60 (4) ◽  
Author(s):  
Tomasz Liberek ◽  
Julita Śliwarska ◽  
Krzysztof Czurak ◽  
Agnieszka Perkowska-Ptasińska ◽  
Ewa Weber ◽  
...  
Keyword(s):  
Renal Failure ◽  
Ethylene Glycol ◽  
Renal Biopsy ◽  
Renal Injury ◽  
Low Dose ◽  
Ethanol Consumption ◽  
Acute Renal Injury ◽  
Ethylene Glycol Poisoning ◽  
Ethylene Glycol Intoxication

Ethylene glycol poisoning is not an uncommon cause of an acute renal injury. In this paper we present case of prolonged renal failure in the course of ethylene glycol intoxication. Due to the low dose of ingested ethylene glycol and concomitant ethanol consumption, the neurodepressive phase of the intoxication was rather mild and patient presented to the hospital on the ninth day after poisoning with established renal failure. The diagnosis of the specific cause of renal injury was facilitated by the renal biopsy.

scholarly journals Feasibility of Peritoneal Dialysis in Extremely Low Birth Weight Infants

2012 ◽  
Vol 1 (4) ◽  
pp. 52 ◽  
Author(s):  
Francesco Macchini ◽  
Agnese De Carli ◽  
Sara Testa ◽  
Rossella Arnoldi ◽  
Stefano Ghirardello ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Peritoneal Dialysis ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Abdominal Wall ◽  
Renal Injury ◽  
Extremely Low Birth Weight ◽  
Acute Renal Injury ◽  
Low Birth Weight Infants

Acute renal injury is common in extremely low birth weight (ELBW) infants with a frequency ranging from 8% to 24%. Peritoneal dialysis (PD) has been used only occasionally in ELBW. We report our experience and share the solutions used to tackle the difficulties rising from the small size of this type of patients. PD was successfully performed in three ELBW infants with acute renal failure. A neonatal, single-cuff, straight Tenckhoff catheter was placed in 2 patients, while a Broviac single cuff vascular catheter was used in another. PD was feasible and effective in all children. Leakage was observed with Tenckhoff catheters, but this didn’t impair the PD efficacy. The technical difficulties were related to the size and shape of the peritoneal catheters, not easily fitting with the very thin abdominal wall of the preterm in­fants. We conclude that PD is feasible and effective, can be considered as the rescue ther­apy in preterm ELBW infants with acute renal failure.

Calpastatin overexpression prevents progression of S-1,2-dichlorovinyl-l-cysteine (DCVC)-initiated acute renal injury and renal failure (ARF) in diabetes

2006 ◽  
Vol 215 (2) ◽  
pp. 146-157 ◽  
Author(s):  
A DNYANMOTE ◽  
S SAWANT ◽  
E LOCK ◽  
J LATENDRESSE ◽  
A WARBRITTON ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Injury ◽  
Acute Renal Injury

Alterations in rabbit renal microvascular prostanoid synthesis in acute renal failure

1988 ◽  
Vol 254 (5) ◽  
pp. F684-F688 ◽  
Author(s):  
A. Chaudhari ◽  
M. A. Kirschenbaum
Keyword(s):  
Renal Failure ◽  
Uranyl Nitrate ◽  
Renal Injury ◽  
Renal Hemodynamics ◽  
Acute Renal Injury ◽  
Alpha Production ◽  
Prostanoid Production ◽  
Prostanoid Synthesis ◽  
Stimulation Of

Vasodepressor prostanoids have been suggested to regulate renal hemodynamics after nephrotoxic injury and thus protect the kidney against the effects of prolonged ischemia. This study assessed whether changes in two microvascular vasodilator prostanoids would correlate with changes seen in renal hemodynamics in rabbits with nephrotoxic renal injury produced by either uranyl nitrate or mercuric chloride. Rabbits were killed at 3, 24, and 72 h after the nephrotoxin injections and 6-ketoprostaglandin (PG) F1 alpha and PGE2 synthesis was measured in vitro in isolated renal microvessels. At the end of 24 h, synthesis of both prostanoids was significantly increased in all nephrotoxin-treated animals, an observation not noted at the end of 3 h. At 72 h, 6-keto-PGF1 alpha production remained elevated. Pretreatment with mepacrine blocked the increased prostanoid production seen in uranyl nitrate-treated animals. Thus, renal microvascular vasodilator prostanoid biosynthesis is increased 24-72 h after nephrotoxin administration. These data suggest that the biosynthesis of prostacyclin and PGE2 may contribute to the maintenance of renal blood flow in the first few days after acute renal injury and further suggest that a mechanism for this increase may be stimulation of phospholipase A2.

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