Drug-induced Kidney Research Articles

Cysteine conjugate of paracetamol serves as substrate for kidney cysteine S-conjugates ß-lyase: implications for drug-induced acute kidney injury

Cysteine conjugate of paracetamol serves as substrate for kidney cysteine S-conjugates ß-lyase: implications for drug-induced acute kidney injury

Острое почечное повреждение, индуцированное лекарствами, среди больных стационара терапевтического профиля

Острое почечное повреждение, индуцированное лекарствами, среди больных стационара терапевтического профиля

A Case of Iodoform Toxicity Due to Drug-Induced Acute Kidney Injury After Discontinuation of Iodoform Gauze.

A Case of Iodoform Toxicity Due to Drug-Induced Acute Kidney Injury After Discontinuation of Iodoform Gauze.

Clinical Characteristics of 162 Patients with Drug-Induced Liver and/or Kidney Injury.

Context Drug-induced liver and kidney injuries are the most common adverse drug reactions in the clinic, and they have similar pathogeneses. Aims To analyze the clinical characteristics of patients with drug-induced liver and/or kidney injury. Settings and Design This was a retrospective study. Methods and Materials We analyzed data from 162 patients with drug-induced liver and/or kidney injury from 2008 to 2018 at the Chinese Rocket Force Characteristic Medical Center. Univariate and multivariate logistic analyses were performed on the drugs used, sex, age, weight, complications, and laboratory test results. Statistical analysis was performed using SPSS 25.0 statistical software. Results (1) The most common drugs causing organ injury in this study were antineoplastic drugs, antibiotics, traditional Chinese medicine, lipid-lowering drugs, and nonsteroidal anti-inflammatory drugs. (2) Among 22 patients with drug-induced liver and kidney injuries, 68.18% had a hepatocellular pattern, 13.64% had a mixed pattern, and 18.18% had a cholestatic pattern. Among the three groups, the P value for creatinine was 0.002. (3) The P value for urinary protein between the isolated kidney injury group and the liver and kidney injury group was 0.028. (4) Multivariate analysis showed that, among the drug-induced renal injury patients and all injury patients, those with a higher neutrophil percentage had a lower risk of liver injury (OR = 0.574, 95% CI: 0.390–0.846; OR = 0.545, 95% CI: 0.396–0.749). Conclusions (1) The serum creatinine level was higher in liver injury patients with the cholestatic pattern than in those with the hepatocellular or mixed pattern. (2) There was a significant difference in urinary protein between the isolated kidney and the liver and kidney injury groups. (3) Among patients with drug-induced organ injury, those with a higher neutrophils percentage had a lower risk of liver injury.

Drug-induced renal disorder-A Mini Review

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.

Renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug-induced acute kidney injury (AKI)

Renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug-induced acute kidney injury (AKI)

Acute kidney injury secondary to the use of methotrexate

This article draws on the case of a 78-year-old man, Mr MC, who was diagnosed with drug-induced acute kidney injury (AKI) as a result of an overdose of methotrexate. Reflecting on this scenario, Adrian Coleman and Melissa Nankoo outline the indications for methotrexate, explore the drug's mechanism of action and discuss how excessive doses of methotrexate can lead to AKI.

Serum lipidomic analysis of an animal model of drug-induced acute kidney injury in rats

Serum lipidomic analysis of an animal model of drug-induced acute kidney injury in rats

Drug-induced acute kidney injury

Due to their physiological function, the kidneys are exposed to high concentrations of numerous drugs and their metabolites, making them vulnerable to drug-related injuries. This article provides an overview of the pathophysiological mechanisms involved in nephrotoxicity, the most common nephrotoxic drugs, and the risk factors for the occurrence of drug-induced acute kidney injuries. NSAIDs, diuretics, ACE inhibitors, and angiotensin II receptor blockers (ARBs} are the most frequent prerenal causes of an acute elevation in creatinine levels. Primary vascular damage arises from thrombotic microangiopathy (e. g. due to cic/osporin, tacrolimus, muromonab-CD3, mitomycin C, quinine, ticlopidine, clopidogrel}. Anticoagulants and thrombolytic medications lead to secondary blood vessel damage by cholesterol emboli, embolism of thrombus material into the periphery or bleeding. Tubulopathies can be observed on treatment with ifosfamide and cisplatin (rarely with cyclophosphamide or carboplatin), aminoglycosides, vancomycin, and radiocontrast agents. Immunological mechanisms underlie interstitial nephritides, which are induced by drugs in about 85% of cases. In drug-induced glomerulopathies;- renal biopsy allows closer identification of the triggering medication. Drug-induced systemic lupus erythematosus (SLE} represents a special form of immune complex glomerulonephritis and can be triggered by procainamide, hydralazine, isoniazid, methyldopa, quinidine, chlorpromazine, and propylthiouracil. Crystal-induced kidney injury is caused by precipitation of drugs (e. g. aciclovir, sulfonamide antibiotics, methotrexate, indinavir) in the renal tubules and the urine-conducting organs with consecutive obstruction thereof.

Preliminary study on general safe medication regularity of Chinese patent orthopedic medicines based on adverse reaction/event literature analysis

Chinese patent orthopedic medicines feature complex components, mainly including desperate and toxic herbal pieces, narrow safety window, more clinical contraindications and frequent adverse drug reaction/events (ADR/ADE). To study the general safe medication regularity of Chinese patent orthopedic medicines, define key points in the medication education and ensure rational clinical medication, the authors took 80 types of commonly used Chinese patent orthopedic medicines as the study objects, collect 237 cases from 164 ADR/ADE documents through a system retrieval strategy, make a multidimensional literature analysis to determine the common risk factors for safe and rational medication of Chinese patent orthopedic medicines and establish an ADR/ADE prevention regularity. First, in the aspect of clinical symptoms, skin allergy is the most common ADR/ADE and closely related to the toxic ingredients, particularly accumulated liver or kidney damage caused by some drugs. Second, there are three time nodes in the ADR/ADE occurrence; The ADR/ADE occurred in 30 minutes is closely related to the idiosyncrasy; the ADR/ADE occurred between several months and half a year is related to the drug-induced liver and kidney damages; The most common ADR/ADE was observed within 7 days and predictable according to the pharmacological actions; Third, toxicity is an important factor in the occurrence of ADR/ADE of Chinese patent orthopedic medicines. Fourth, emphasis shall be given to the special medication factors, such as the combination with western medicines and Chinese herbal decoctions, overdose and long-course medication and self-medical therapy. In conclusion, the general ADR/ADE prevention regularity for Chinese patent orthopedic medicines was summarized to provide supports for clinicians in safe and rational medication and give the guidance for pharmacist in medication education.

The causes of drug-induced acute kidney injury

Caroline Ashley gives an overview of drug-induced acute kidney injury (AKI), listing the causes and drugs that can potentially injure the kidneys and explaining the mechanisms by which the injury may be caused. Knowing the risk factors that increase the incidence of AKI after drug exposure and taking measures that help reduce risks will help prevent this potentially life-threatening emergency.

Neuroprotection by the α 2-adrenoceptor agonist, dexmedetomidine, in rat focal cerebral ischemia

The present study was undertaken to explore the possible neuroprotective effect of the selective α 2-adrenoceptor agonist, dexmedetomidine in a rat model of focal cerebral ischemia. The effect of dexmedetomidine (9 μg kg −1) on infarct volume was assessed and compared to that of glutamate receptor antagonists cis-4(phosphonomethyl)-2-piperidine carboxylic acid (CGS-19755) (20 mg kg −1) or 2,3-dihydro-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX) (50 mg kg −1). Dexmedetomidine decreased total ischemic volume by 40% in the cortex ( P<0.05) compared to NaCl-treated control rats, whereas NBQX reduced the infarct by 73% in the cortex ( P<0.001) and by 43% in the striatum ( P<0.01). Dexmedetomidine infusion was associated with some minor degree of hyperglycemia and hypotension. Drug-induced kidney changes were only seen in NBQX-treated rats. These results suggest that dexmedetomidine reduced ischemic volume despite causing a minor increase in blood glucose concentrations and hypotension. Its neuroprotective efficacy was better than that produced by CGS-19775, and dexmedetomidine was safer with respect to kidney toxicity when compared to NBQX.