Antiviral Drugs and Acute Kidney Injury (AKI)

2019 ◽  
Vol 19 (4) ◽  
pp. 375-382 ◽  
Author(s):  
Wattana Leowattana

The introduction of more efficient antiviral drugs are common cause drug-induced acute kidney injury (AKI). The true prevalence of antiviral drugs induced nephrotoxicity is hardly determined. It causes AKI by many mechanisms including acute tubular necrosis (ATN), allergic interstitial nephritis (AIN), and crystal nephropathy. ATN has been described with a few kinds of antiviral drugs such as cidofovir, adefovir and tenofovir with unique effects on transporter defects, apoptosis, and mitochondrial injury. AIN from atazanavir is a rapid onset of AKI and usually nonoliguric but dialytic therapy are needed because of severity. Additionally, crystal nephropathy from acyclovir, indinavir, and foscarnet can cause AKI due to intratubular obstruction. In this article, the mechanisms of antiviral drug-induced AKI were reviewed and strategies for preventing AKI were mentioned.

2019 ◽  
Vol 2 (3) ◽  
pp. 164-168
Author(s):  
Amrit KC ◽  
Rahman Tanvir ◽  
Alam Muhammad Rafiqul ◽  
Ahmed A.H. Hamid ◽  
Noor Towhida

Background: Though peritoneal dialysis has several limitations, it is still used in acute kidney injury (AKI) patients as an alternative method of Renal Replacement Therapy (RRT), especially in low socioeconomic countries. Materials and Method: This study included thirty patients diagnosed as AKI. Peritoneal access was established through flexible Tenckhoff catheter for Continuous Peritoneal Dialysis (CPD) and 6-8 exchanges were done in 24 hours. Results: Among 30 patients mean age was (mean±SD) 49.93±14.42 years. Seven (23.33%) patients were hemodynamically unstable. The cause of AKI was drug induced in 6(20.7%), hypovolemia/Acute Tubular Necrosis in 6(20.0%), sepsis in 5(16.7%), heart failure in 2(6.7%) and 11(36.7%) had multiple causes. In initial presentation, mean serum creatinine was 683.42 μmol/L, and the number of sessions required for stabilization of serum creatinine was 7.5±1.43, sessions required for correction of hyperkalemia and metabolic acidosis were 2.15±0.69 and 2.5±0.76 respectively. The delivered Kt/V urea was 1.95±0.14 weekly. Six (20.0%) patients had peritonitis, five (16.7%) had pericatheter leakage and four (13.33%) had catheter blockage. Among 30 patients, three patients (10%) had died, sixteen (59.3%) had recovery of renal function and rest did not recover renal function. Conclusion: CPD was effective for correction of metabolic and electrolyte imbalance.  


2019 ◽  
Vol 72 (8) ◽  
pp. 1466-1472
Author(s):  
Grażyna Kobus ◽  
Jolanta Małyszko ◽  
Hanna Bachórzewska-Gajewska

Introduction: In the elderly, impairment of kidney function occurs. Renal diseases overlap with anatomic and functional changes related to age-related involutionary processes. Mortality among patients with acute renal injury is approximately 50%, despite advances in treatment and diagnosis of AKI. The aim: To assess the incidence of acute kidney injury in elderly patients and to analyze the causes of acute renal failure depending on age. Materials and methods: A retrospective analysis included medical documentation of patients hospitalized in the Nephrology Clinic during the 6-month period. During this period 452 patients were hospitalized in the clinic. A group of 77 patients with acute renal failure as a reason for hospitalization was included in the study. Results: The prerenal form was the most common cause of AKI in both age groups. In both age groups, the most common cause was dehydration; in the group of patients up to 65 years of age, dehydration was 29.17%; in the group of people over 65 years - 43.39%. Renal replacement therapy in patients with AKI was used in 14.29% of patients. In the group of patients up to 65 years of age hemodialysis was 16.67% and above 65 years of age. -13.21% of patients. The average creatinine level in the group of younger patients at admission was 5.16 ± 3.71 mg / dl, in the group of older patients 3.14 ± 1.63 mg / dl. The size of glomerular filtration GFR in the group of younger patients at admission was 21.14 ± 19.54 ml / min, in the group of older patients 23.34 ± 13.33 ml / min. Conclusions: The main cause of acute kidney injury regardless of the age group was dehydration. Due to the high percentage of AKI in the elderly, this group requires more preventive action, not only in the hospital but also at home.


2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.


2021 ◽  
Vol 10 (2) ◽  
pp. 168
Author(s):  
Anne-Lise Rolland ◽  
Anne-Sophie Garnier ◽  
Katy Meunier ◽  
Guillaume Drablier ◽  
Marie Briet

Background: Acute kidney injury (AKI) is a public health concern. Among the pathological situations leading to AKI, drugs are preventable factors but are still under-notified. We aimed to provide an overview of drug-induced AKI (DIAKI) using pharmacovigilance and medical administrative databases Methods: A query of the PMSI database (French Medical Information System Program) of adult inpatient hospital stays between 1 January 2017 and 31 December 2018 was performed using ICD-10 (International Classification of Diseases 10th revision) codes to identify AKI cases which were reviewed by a nephrologist and a pharmacovigilance expert to identify DIAKI cases. In parallel, DIAKIs notified in the French Pharmacovigilance Database (FPVDB) were collected. A capture-recapture method was performed to estimate the total number of DIAKIs. Results: The estimated total number of DIAKIs was 521 (95%CI 480; 563), representing 20.0% of all AKIs. The notification was at a rate of 12.9% (95%CI 10.0; 15.8). According to the KDIGO classification, 50.2% of the DIAKI cases were stage 1 and 49.8% stage 2 and 3. The mortality rate was 11.1% and 9.6% required hemodialysis. Conclusion: This study showed that drugs are involved in a significant proportion of patients developing AKI during a hospital stay and emphasizes the severity of DIAKI cases.


2015 ◽  
Vol 11 (11) ◽  
pp. 1683-1694 ◽  
Author(s):  
Glenda C Gobe ◽  
Jeff S Coombes ◽  
Robert G Fassett ◽  
Zoltan H Endre

2021 ◽  
Vol 546 ◽  
pp. 103-110
Author(s):  
Masayoshi Saito ◽  
Satoshi Horie ◽  
Hidenori Yasuhara ◽  
Akane Kashimura ◽  
Eiji Sugiyama ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
pp. 42-48
Author(s):  
Ali Ayaash ◽  
Dipesh Maan ◽  
Anastasios Kapetanos ◽  
Mark Bunker ◽  
Mary Chester Wasko ◽  
...  

Crescentic glomerulonephritis (GN) without immune reactants or deposits (referred to as pauci-immune) is typically characterized by the presence of anti-neutrophilic cytoplasmic antibodies (ANCA). While ANCA-negative patients might be expected to have a more benign course, they often have poor renal outcomes, especially without treatment with steroids and immune-modulating therapy. Pauci-immune crescentic GN can also co-exist with other autoimmune conditions, including rheumatoid arthritis (RA). Here, we describe an ANCA-negative patient with RA who developed dialysis-requiring acute kidney injury (AKI) with findings consistent with focal pauci-immune crescentic GN (i.e., no IgG or immune complex on kidney biopsy). Coexistent conditions included Klebsiella sepsis attributed to pneumonia, rhabdomyolysis, leukocytoclastic immune-mediated skin vasculitis, and positive ANA. He had spontaneous improvement in renal function without immunosuppressive therapy. This crescentic GN was not associated with poor renal outcome as AKI resolved with supportive care and treatment of his infection. The AKI was likely multifactorial with co-existing acute tubular necrosis in the setting of Kebsiella sepsis and rhabdomyolysis, and the crescentic GN was felt more likely to be related to the infection rather than having a primary role. This case highlights the importance of viewing crescentic GN in the context of the clinical picture, as it may not always lead to the need of aggressive immune suppression and is not a universally poor prognostic kidney finding. However, these cases do warrant close follow-up as our patient had recurrent RA disease manifestations over the next 2 years that eventually led to his death from severe pulmonary hypertension.


2020 ◽  
Vol 58 (228) ◽  
Author(s):  
Pukar Thapa ◽  
Sudhamshu KC ◽  
Achyut Bikram Hamal ◽  
Dilip Sharma ◽  
Sandip Khadka ◽  
...  

Introduction: Acute kidney injury is a common and life-threatening event in patients with liver cirrhosis occurring in approximately 20-50% of hospitalized patients of liver cirrhosis. Pre-renal acute kidney injury, the hepatorenal syndrome type of acute kidney injury and acute tubular necrosis represent the common causes. The aim of this study was to study the profile of acute kidney injury in patients with liver cirrhosis. Methods: Consecutive patients of liver cirrhosis admitted in Liver unit of Bir Hospital were studied to see the presence of acute kidney injury in this hospital based descriptive cross-sectional study. Clinical and laboratory parameters along with various clinical outcome were compared between different groups categorized by the severity of liver disease and renal dysfunction. Results: Out of 302 liver cirrhosis patients, 56 (18.5%) had acute kidney injury among which 23 (46%) were found to have pre-renal acute kidney injury, 15 (30%) with hepatorenal syndrome– acute kidney injury and 12 (24%) with intrinsic renal disease. Patients with higher stages of acute kidney injury had longer duration of hospital stay and hepatorenal syndrome-acute kidney injury was seen in patients with higher grade of ascites and with hyponatremia. Conclusions: Acute kidney injury is a common occurrence in patients with advanced liver cirrhosis with pre-renal acute kidney injury being the commonest cause. Median hospital stay is directly affected by the severity of acute kidney injury and hepatorenal syndrome–acute kidney injury was seen in patients with higher grade of ascites and hyponatremia. Early identification of patients at high risk for acute kidney injury may help to reduce mortality and contain costs.  


2021 ◽  
Author(s):  
Arshpal Gill ◽  
Ra’ed Nassar ◽  
Ruby Sangha ◽  
Mohammed Abureesh ◽  
Dhineshreddy Gurala ◽  
...  

Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in cirrhotic patients, and the management HRS.


2014 ◽  
Vol 280 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Xiaobing Zhou ◽  
Ben Ma ◽  
Zhi Lin ◽  
Zhe Qu ◽  
Yan Huo ◽  
...  

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