Deleterious effects of gentamicin and cisplatin on renal function in rats and early detection of drug-induced kidney injury using biomarkers

2013 ◽  
Vol 68 (1) ◽  
pp. e51-e52
Author(s):  
Eric Delpy ◽  
Marine Habault ◽  
Catherine Le Quement ◽  
Christophe Drieu La Rochelle
Keyword(s):  
Renal Function ◽  
Early Detection ◽  
Kidney Injury ◽  
Drug Induced

Metabolomics for early detection of drug-induced kidney injury: review of the current status

Bioanalysis ◽  
2009 ◽  
Vol 1 (9) ◽  
pp. 1645-1663 ◽  
Author(s):  
Kurt J Boudonck ◽  
Donald J Rose ◽  
Edward D Karoly ◽  
Douglas P Lee ◽  
Kay A Lawton ◽  
...  
Keyword(s):  
Early Detection ◽  
Kidney Injury ◽  
Current Status ◽  
Drug Induced

scholarly journals Drug-induced renal disorder-A Mini Review

2020 ◽  
Vol 11 (1) ◽  
pp. 166-172 ◽  
Author(s):  
Divya M ◽  
Nivetha S. R. ◽  
Lekshmi Mohan ◽  
Arul B* ◽  
Kothai R
Keyword(s):  
Risk Factors ◽  
Renal Function ◽  
Renal Dysfunction ◽  
Renal Scarring ◽  
Kidney Injury ◽  
Drug Induced ◽  
Related Factors ◽  
Renal Disorder ◽  
Renal Obstruction ◽  
Renal Tubular Cells

Drug-induced kidney disorder/disease (DKID) is an origin of kidney disease followed by acute renal failure. Drug-induced renal toxicity is more common in infants and young children in certain clinical circumstances where underlying renal dysfunction and cardiovascular diseases. Sometimes, administered drugs may cause acute renal injury, intra-renal obstruction, interstitial nephritis, nephrotic syndrome, and acid-base and fluid electrolytes disorders in patients. Certain drugs may cause alterations in intra-glomerular hemodynamics, inflammatory changes in renal tubular cells, leading to acute kidney injury (AKI), interstitial tubule disease, and renal scarring. Common risk factors include; pre-existing renal dysfunction, volume-depleted state, old age, and use of nephrotoxic drugs. Therefore, the prevention from the disease includes the knowledge about the nephrotoxicity, assessing considering the patient-related, kidney-related, and drug-related factors while prescribing medicines, using of alternative drugs, which are non-nephrotoxic, assessing the baseline of renal function before starting the treatment, monitor the renal function during the treatment and avoid the nephrotoxic drug combinations and withdrawing the offending drugs due to toxicity. The ADRs of the prescribed/ administered are identified at the earliest to prevent the development of the last-stage renal disorder. This review discusses the risk factors associated with drug-induced renal disease, estimation of renal function, mechanism of drug-induced nephrotoxicity, and certain drugs that cause nephrotoxicity.

Multiplex Optical Urinalysis for Early Detection of Drug-Induced Kidney Injury

2020 ◽  
Vol 92 (8) ◽  
pp. 6166-6172 ◽  
Author(s):  
Penghui Cheng ◽  
Qingqing Miao ◽  
Jiaguo Huang ◽  
Jingchao Li ◽  
Kanyi Pu
Keyword(s):  
Early Detection ◽  
Kidney Injury ◽  
Drug Induced

scholarly journals Nephroprotective Effects of Dioscoreaalata and Moriengaolifera on Cisplatin Induced Nephrotoxicity in Rats

2019 ◽  
Vol 31 (1) ◽  
pp. 46-51
Author(s):  
AKM Shahidur Rahman ◽  
Anwar Habib ◽  
Nishat Parvin ◽  
Monjurur Rahman Shah Chowdhury
Keyword(s):  
Renal Function ◽  
Medicinal Plant ◽  
Plant Extracts ◽  
Vital Signs ◽  
Kidney Injury ◽  
Toxic Effects ◽  
Common Source ◽  
Drug Induced ◽  
Pathogenic Mechanisms ◽  
Medicinal Plant Extracts

Nephrotoxicity, which is caused by mostly due to medication, is one of most important global health problem. Drugs are a common source of acute kidney injury. Drugs shown to cause nephrotoxicity exert their toxic effects by one or more common pathogenic mechanisms. . Most drugs found to cause nephrotoxicity exert toxic effects by one or more common pathogenic mechanisms. These include altered intraglomerular hemodynamics, tubular cell toxicity, inflammation, crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy. Drug-induced nephrotoxicity tends to be more common among certain patients and in specific clinical situations. Cisplatin, one of the many drugs, is responsible for severe nephrotoxicity. General preventive measures to avoid nephrotoxicity include using alternative non-nephrotoxic drugs; correcting risk factors; assessing baseline renal function before initiation of therapy, followed by adjusting the dosage; monitoring renal function and vital signs during therapy; and avoiding nephrotoxic drug combinations, using of several nephroprotective agents including medicinal plant extracts. Promising results showed that the use of some medicinal plant extracts (Dioscoreaalata and Moriengaolifera) gave rise to moderate restoration of normal physiology of kidney and liver of mice. TAJ 2018; 31(1): 46-51

scholarly journals Outcome of Continuous Peritoneal Dialysis in Patient with Acute Kidney Injury

2019 ◽  
Vol 2 (3) ◽  
pp. 164-168
Author(s):  
Amrit KC ◽  
Rahman Tanvir ◽  
Alam Muhammad Rafiqul ◽  
Ahmed A.H. Hamid ◽  
Noor Towhida
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Peritoneal Dialysis ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Electrolyte Imbalance ◽  
Drug Induced ◽  
Low Socioeconomic ◽  
Tubular Necrosis ◽  
Continuous Peritoneal Dialysis

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.  

scholarly journals Bile Cast Nephropathy: The Unknown Dangers of Online Shopping

2018 ◽  
Vol 8 (2) ◽  
pp. 98-102 ◽  
Author(s):  
Andrea Fisler ◽  
Tobias Breidthardt ◽  
Nadine Schmidlin ◽  
Helmut Hopfer ◽  
Michael Dickenmann ◽  
...  
Keyword(s):  
Renal Function ◽  
Early Recognition ◽  
Anabolic Steroids ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Cholestatic Liver Disease ◽  
Renal Tubules ◽  
Volume Depletion ◽  
Drug Induced ◽  
Cast Nephropathy

Renal dysfunction in the setting of cholestatic liver disease is multifactorial but most often due to decreased kidney perfusion from intravascular volume depletion, acute tubular injury/necrosis, and hepatorenal syndrome. Drug-induced hepatotoxicity may be associated with a cholestatic injury pattern. We report a case of a 56-year-old man with a diagnosis of bile cast nephropathy, as a complication of drug-induced severe hyperbilirubinemia due to the abuse of intramuscular anabolic steroids bought on the internet to increase muscular mass for bodybuilding training. Kidney biopsy showed the histological pattern of diffuse potentially reversible tubular damage with intratubular bile casts obstructing the renal tubules. The patient developed acute kidney injury and needed dialysis treatment for 4 weeks until renal function recovered. The severity of the kidney injury and the requirement of hemodialysis observed in our patient are unique and have not been previously described. As full recovery of renal function is suspected with decreasing bilirubin levels, early recognition and treatment of the underlying disease is essential.

Acute interstitial nephritis

2020 ◽  
pp. 4951-4956
Author(s):  
Simon D. Roger
Keyword(s):  
Renal Function ◽  
Interstitial Nephritis ◽  
Lupus Erythematosus ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Sudden Onset ◽  
Rapid Decline ◽  
Drug Induced ◽  
Chronic Renal Impairment ◽  
Loin Pain

Acute interstitial nephritis (AIN) is an inflammation of the tubules and interstitium within the kidney, associated with a relatively sudden onset and rapid decline in renal function. It is usually secondary to drugs (antibiotics, nonsteroidal anti-inflammatory drugs, and proton pump inhibitors being most commonly incriminated), with other causes being infections (classically streptococcal, but this is now less common) and immune disorders (systemic lupus erythematosus, sarcoidosis, and tubulointerstitial nephritis with uveitis). Clinical features—the diagnosis of AIN should be considered in any patient with unexplained acute kidney injury. Drug-induced AIN may present with a classic allergic response, including arthralgias, fever, rash, loin pain, and eosinophilia/eosinophiluria, but these are not invariable and their absence does not exclude the diagnosis. The urine typically shows low-grade proteinuria (<1 g/day). Renal biopsy is the only way to confirm or exclude the diagnosis. Management and prognosis—treatment is by ceasing the offending agent, treating the concurrent infectious cause, or managing the immune aetiology with steroids (typically prednisolone 1 mg/kg per day, tapered to zero over 6–8 weeks). Most patients with drug-induced AIN recover renal function, but some are left with chronic renal impairment and a small proportion progress to endstage chronic kidney disease.

scholarly journals Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

2020 ◽  
Author(s):  
Jing Zhou ◽  
Xiaojuan Yu ◽  
Tao Su ◽  
Suxia Wang ◽  
Li Yang
Keyword(s):  
Renal Function ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Tubular Injury ◽  
Early Recovery ◽  
Drug Induced ◽  
Crystal Deposition ◽  
Common Cause ◽  
Acute Kidney Disease

Abstract Backgrounds: This study aimed to summarize and analyze the clinicopathological features of acute kidney disease patients with renal oxalosis, to improve understanding of the disease characteristics. Methods: Data for patients with acute kidney disease (AKD) diagnosed from January 2011 to October 2018 and confirmed by renal biopsy showing oxalate crystal deposition were collected. The underlying diseases, dietary habits before disease onset, pathological characteristics of newly emerging kidney disease, renal oxalosis, and causes of AKD were analyzed. Urine volume, serum creatinine, uric acid, and electrolyte clearance were recorded. The long-term renal prognosis was observed. Results: A total of 23 patients with AKD and renal oxalosis were included. The patients comprised 18 men (78.3%) and 5 women (21.7%) with a mean age of 51.6 ± 15.9 years. The peak serum creatinine was 669.9 ± 299.8 μmol/L, and 95.7% of patients had stage 3 acute kidney injury. Drug-induced AKD was the most common cause (65.2%), followed by severe nephrotic syndrome (17.4%). Other causes included severe glomerulonephritis, and infection. All patients had pathological changes indicating tubulointerstitial disease (TIN), and 11 patients were complicated with newly emerging glomerular disease (GD). Oxalate deposits caused by increased enterogenous oxalate absorption accounted for 26.1%, and most of the causes came from new kidney diseases. Oxalate crystals were located in the renal tubule. The majority (75%) of moderate to severe oxalate crystal deposition occurred in patients without GD. There were no significant differences in the total score for acute tubulointerstitial injury, score for tubular injury (T-IS), and score for interstitial inflammation in patients with different severities of renal oxalosis. Rate of serum creatinine decrease (ΔScr%) was negatively correlated with severity of oxalosis (R = −0.542, P = 0.037), score for acute tubular injury (R = −0.553, P = 0.033), and age (R = −0.736, P = 0.002). ΔScr% at week 4 was correlated with T-IS (R = −0.433, P = 0.050), but was not correlated with severity of oxalosis. Conclusions: The present findings revealed that 95.7% of AKD cases with renal oxalosis occurred in critically ill patients, secondary to kidney injury with tubular injury, and that drug-induced AKD was the most common cause. Severe oxalosis contributed to delayed early recovery of renal function.

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