Renal medicine

2012 ◽  
pp. 383-402
Author(s):  
Lesley K Bowker ◽  
James D Price ◽  
Sarah C Smith
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Replacement Therapy ◽  
Filtration Rate ◽  
Fluid Challenge ◽  
Kidney Injury ◽  
Injury Management

The ageing kidney 384 Acute kidney injury 386 Acute kidney injury: management 388 HOW TO . . . Perform a fluid challenge in AKI/anuria 389 Chronic kidney disease 392 HOW TO . . . Estimate the glomerular filtration rate 393 Chronic kidney disease: complications 394 Renal replacement therapy: dialysis 396 Renal replacement therapy: transplantation ...

Renal medicine

2018 ◽  
Author(s):  
Lesley K. Bowker ◽  
James D. Price ◽  
Ku Shah ◽  
Sarah C. Smith
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Nephrotic Syndrome ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Renal Artery ◽  
Replacement Therapy ◽  
Renal Artery Stenosis ◽  
Kidney Injury ◽  
Injury Management

This chapter provides information on the ageing kidney, acute kidney injury, management of acute kidney injury, chronic kidney disease, complications of chronic kidney disease, dialysis in renal replacement therapy, transplantation in renal replacement therapy, nephrotic syndrome, glomerulonephritis, and renal artery stenosis.

scholarly journals The Clinical Utility of Kinetic Glomerular Filtration Rate in the Assessment of Renal Function and Prediction of Outcomes Among Critically Ill Patients With Acute Kidney Injury: A Single-Center Retrospective Cohort Study

2021 ◽  
Vol 5 (1) ◽  
pp. 611-620
Author(s):  
Shari Ann Atanacio ◽  
Maria Rachel Uy
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Peritoneal Dialysis ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Replacement Therapy ◽  
Urine Output ◽  
Filtration Rate ◽  
Kidney Injury

Objective: To determine the discriminatory ability of kinetic glomerular filtration rate (kGFR) to detect acute kidney injury (AKI) when compared with established GFR equations and criteria and relating it to mortality, renal replacement therapy initiation and renal recovery. Methods: This was a retrospective analysis using data from chart review of 109 intensive care unit (ICU) patients at the University of Santo Tomas Hospital (USTH). The renal function estimates using Chronic Kidney Disease Epidemiology Collaboration (CKD-Epi), modification of diet in renal disease (MDRD), Kidney Disease Improving Global Outcomes Acute Kidney Injury (KDIGO AKI), as well as kinetic GFR equations were compared and correlated with renal and cardiovascular outcomes. Results: The renal function assessed by kGFR, CKD-Epi, MDRD and KDIGO staging based on serum creatinine (SCr) showed no significant association with mortality outcomes. However, AKI diagnosed based on urine output (UO), and combined SCr and urine output (KDIGO) showed association with all-cause mortality. The UO detected severe stages of AKI while SCr (based on KDIGO) better identified the earlier stages of AKI. The criteria for KDIGO AKI when combined also shows mortality prediction since it joins together the effects of SCr and UO. There was a remarkable 3.5 times increase  in hemodialysis initiation (p=0.0001) and 12.89 times increase in peritoneal dialysis initiation (p=0.01) for every stage increase in the KDIGO classification. kGFR, CKD-Epi and MDRD have 5%, 6%, and 6% decrease, respectively in the odds of initiating hemodialysis. There was however, no association for peritoneal dialysis. Conclusion: kGFR was the least able in detecting AKI and KDIGO AKI criteria remains to be the standard in identifying AKI in the critical care setting. Increase in SCr was a sensitive tool in diagnosing AKI due to its ability to detect AKI based on a small increase in SCr regardless of the baseline renal function. Decreasing UO, however, is the prognosticating variable in KDIGO AKI criteria, in that it portends higher probability of initiation of renal replacement therapy (RRT) and ultimately higher mortality when present.

scholarly journals New mouse model of chronic kidney disease transitioned from ischemic acute kidney injury

2019 ◽  
Vol 317 (2) ◽  
pp. F286-F295 ◽  
Author(s):  
Jin Wei ◽  
Jie Zhang ◽  
Lei Wang ◽  
Shan Jiang ◽  
Liying Fu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Reperfusion Injury ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury

Acute kidney injury (AKI) significantly increases the risk of development of chronic kidney disease (CKD), which is closely associated with the severity of AKI. However, the underlying mechanisms for the AKI to CKD transition remain unclear. Several animal models with AKI to CKD transition have been generated and widely used in research; however, none of them exhibit the typical changes in glomerular filtration rate or plasma creatinine, the hallmarks of CKD. In the present study, we developed a novel model with a typical phenotype of AKI to CKD transition in C57BL/6 mice. In this model, life-threatening ischemia-reperfusion injury was performed in one kidney, whereas the contralateral kidney was kept intact to maintain animal survival; then, after 2 wk of recovery, when the renal function of the injured kidney restored above the survival threshold, the contralateral intact kidney was removed. Animals of this two-stage unilateral ischemia-reperfusion injury model with pedicle clamping of 21 and 24 min exhibited an incomplete recovery from AKI and subsequent progression of CKD with characteristics of a progressive decline in glomerular filtration rate, increase in plasma creatinine, worsening of proteinuria, and deleterious histopathological changes, including interstitial fibrosis and glomerulosclerosis. In conclusion, a new model of the AKI to CKD transition was generated in C57BL/6 mice.

Malignancy-associated kidney disease

2016 ◽  
Vol 6 (1) ◽  
pp. 0-0
Author(s):  
K Kozłowska ◽  
J. Małyszko
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Nephrotic Syndrome ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Replacement Therapy ◽  
Tubulointerstitial Nephritis ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Electrolyte Abnormalities

Malignancy or its treatment affect kidney in several ways. The most common are acute kidney injury and chronic kidney disease. Other form of kidney diseases can also be present such as nephrotic syndrome, tubulointerstitial nephritis, thrombotic microangipathy etc. In addition, electrolyte abnormalities such as hypercalcemia, hyponatremia and hypernatremia, hypokalemia and hyperkalemia, and hypomagnesemia. are observed. Treatment of malignancy associated kidney disease is usually symptomatic. Cessation of the offending agent or other supportive measures if needed i.e. renal replacement therapy are also implemented.

Refractory Dabigatran-Induced Hemorrhage Despite Multiple Idarucizumab Administration and Renal Replacement Therapy

2020 ◽  
pp. 089719002096169
Author(s):  
Francis Flynn ◽  
Guillaume Richard ◽  
Marc A. Dobrescu ◽  
Josée Bouchard ◽  
David Williamson ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Replacement Therapy ◽  
Dabigatran Etexilate ◽  
Rebound Effect ◽  
Kidney Injury ◽  
Intermittent Hemodialysis ◽  
Thrombin Time

Purpose: This case report describes a patient with dabigatran accumulation due to acute kidney injury on chronic kidney disease, requiring multiple administration of idarucizumab along with renal replacement therapy because of rebound effect causing numerous episodes of bleeding. Summary: An 86-year-old man on dabigatran etexilate 110 mg twice daily for stroke prevention with atrial fibrillation was admitted to the hospital for bowel obstruction and severe acute kidney injury on chronic kidney disease. The patient had an abnormal coagulation profile and no history of bleeding. Initial laboratory values revealed a hemoglobin concentration of 10.7 g/dL, a platelet count of 115 × 103 platelets/μL, an activated partial thromboplastin time of 150.4 seconds, an international normalized ratio of 10.28, a thrombin time greater than 100 seconds and a serum creatinine of 5.54 mg/dL (490 μmol/L). An initial dose of idarucizumab was administered 1 hour prior to surgery to prevent bleeding. Significant bleeding and hemodynamic instability occurred following surgery. Three additional doses of idarucizumab, 2 sessions of intermittent hemodialysis, continuous venovenous hemofiltration and blood products were required to achieve normalization of coagulation parameters and hemodynamic stability due to rebound coagulopathy after each dose of idarucizumab. Conclusion: Acute kidney injury on chronic kidney disease and third-space redistribution could have led to important dabigatran accumulation and favored rebound coagulopathy. Multiple therapeutic approaches may be required in the management of complex dabigatran intoxication.

FREQUENCY RISK FACTORS AND OUTCOMES ACUTE KIDNEY INJURY IN THE EARLY PERIOD IN PATIENTS WITH CHRONIC KIDNEY DISEASE AFTER CABG SURGERY

2018 ◽  
Vol 22 (4) ◽  
pp. 96-101 ◽  
Author(s):  
V. V. Bazylev ◽  
A. A. Gornostaev ◽  
A. A. Schegol’kov ◽  
A. V. Bulygin
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Bypass Graft ◽  
Early Period ◽  
Kidney Injury

AIM: To evaluate risk factors and prevalence of acute kidney injury (AKI) in patients with chronic kidney disease (CKD) in the early period after isolated coronary artery bypass graft (CABG).PATIENTS AND METHODS:The study included 830 patients with  isolated CABG. All surgeries were performed in 2016. To evaluate  kidney function in preoperative period glomerular filtration rate  (GFR) was estimated by Chronic Kidney Disease Epidemiology  Collaboration (CKD-EPI) formula. AKI was diagnosed according to  KDIGO criteria. Patients were stratified into two groups according to  estimated glomerular filtration rate (eGFR).RESULTS:The prevalence of AKI in patients group without CKD after CABG was 11,5% (n=59), in CKD-AKI group – 12,3% (n=39).  In patients with CKD and after intraoperative inotropic/vasopressor  therapy use of only 2 medicinal drugs of this group the probability of  AKI development increases 11,16 times (OR 11,46; 95% CI 3,47- 37,83; р<0,01). During complete bypass (CB) when haematocrit  decreases on 1% AKI probability increases on 12,36% (OR 0,89; 95% CI 0,81-0,98; р=0,02). The necessity of haemodialisys,  duration of stay in intensive care unit and hospitalization duration  were equal to all groups. AKI-CKD development significantly increases intrahospital mortality (p<0,05). CONCLUSIONS: History of CKD increases probability of severe AKI and also mortality in early postoperative period. Revealed risk factors for AKI development are potentially modifiable.

scholarly journals Beyond the tubule: pathological variants of LRP2, encoding the megalin receptor, result in glomerular loss and early progressive chronic kidney disease

2020 ◽  
Vol 319 (6) ◽  
pp. F988-F999
Author(s):  
Jennifer R. Charlton ◽  
Weizhen Tan ◽  
Ghaleb Daouk ◽  
Lisa Teot ◽  
Seymour Rosen ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Glomerular Proteinuria ◽  
Increased Risk ◽  
Kidney Injury Molecule 1 ◽  
Deficient Mice

Pathogenic variants in the LRP2 gene, encoding the multiligand receptor megalin, cause a rare autosomal recessive syndrome: Donnai-Barrow/Facio-Oculo-Acoustico-Renal (DB/FOAR) syndrome. Because of the rarity of the syndrome, the long-term consequences of the tubulopathy on human renal health have been difficult to ascertain, and the human clinical condition has hitherto been characterized as a benign tubular condition with asymptomatic low-molecular-weight proteinuria. We investigated renal function and morphology in a murine model of DB/FOAR syndrome and in patients with DB/FOAR. We analyzed glomerular filtration rate in mice by FITC-inulin clearance and clinically characterized six families, including nine patients with DB/FOAR and nine family members. Urine samples from patients were analyzed by Western blot analysis and biopsy materials were analyzed by histology. In the mouse model, we used histological methods to assess nephrogenesis and postnatal renal structure and contrast-enhanced magnetic resonance imaging to assess glomerular number. In megalin-deficient mice, we found a lower glomerular filtration rate and an increase in the abundance of injury markers, such as kidney injury molecule-1 and N-acetyl-β-d-glucosaminidase. Renal injury was validated in patients, who presented with increased urinary kidney injury molecule-1, classical markers of chronic kidney disease, and glomerular proteinuria early in life. Megalin-deficient mice had normal nephrogenesis, but they had 19% fewer nephrons in early adulthood and an increased fraction of nephrons with disconnected glomerulotubular junction. In conclusion, megalin dysfunction, as present in DB/FOAR syndrome, confers an increased risk of progression into chronic kidney disease.

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