Acute interstitial nephritis: a multifaceted disease

Chamarthi, Gajapathiraju; Kamboj, Mayanka; Olaoye, Olanrewaju A; Xu, Zhiyong; Koratala, Abhilash

doi:10.1002/ccr3.1456

Cited by 6 publications

(3 citation statements)

References 6 publications

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“…The time from exposure to appearance of symptoms is widely variable and can be from a few days to years. [22,23] In the current study, the patient only took valsartan 40 mg daily. We thought the low dose of drug postponed the occurrence of AIN.…”

Section: Discussionmentioning

confidence: 99%

Severe acute interstitial nephritis induced by valsartan

Chen

et al. 2019

Medicine

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Rationale: Angiotensin receptor blocker (ARB) can increase serum creatinine or potassium levels in patients with renal insufficiency, renal artery stenosis, heart failure or hypovolemia, but hardly cause severe kidney injury in patients without any risk factors. A case of severe acute interstitial nephritis (AIN) induced by valsartan was reported here. Patient concerns: A 62-year-old female with nausea for 1 month and acute deterioration of kidney function for 2 weeks was admitted. She had a history of hypertension for 5 months and had taken valsartan 40 mg daily for 4 months. Although the valsartan had been stopped for 2 weeks, the serum creatinine continuously increased after admission. Kidney biopsy demonstrated the eosinophils infiltration in interstitium. Diagnoses: AIN induced by valsartan. Interventions: The patient was treated with glucocorticoid. Outcomes: The serum creatinine decreased gradually and got back to normal level 5 months later. Then therapy of glucocorticoid was stopped. Renal artery stenosis was excluded by computed tomography angiography (CTA). Lessons: Although valsartan-induced allergy has been reported previously, AIN was firstly recognized as a severe complication of this drug. We suggest when there is a ARB-associated continuous deterioration of kidney function for patients without renal insufficiency, renal artery stenosis, heart failure or hypovolemia, AIN should be thought of and therapy with glucocorticoid should be considered if necessary.

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Section: Discussionmentioning

confidence: 99%

Severe acute interstitial nephritis induced by valsartan

Chen

et al. 2019

Medicine

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“…In the more distal parts of the tubules, drugs may precipitate, crystallize, or form casts, which lead to tubular obstruction [ 9 ]. Another mechanism entails the development of tubulointerstitial inflammation-causing interstitial nephritis [ 10 ]. In summary, drug-induced nephrotoxicity develops according to one of the three mechanisms: (1) proximal tubular injury and acute tubular necrosis (ATN) (a dose-dependent mechanism) via apical contact with drugs or their metabolites, the transport of drugs and their metabolites from the apical surface, and the secretion of drugs from the basolateral surface into the tubular lumen; (2) tubular obstruction by crystals or casts containing drugs and their metabolites (a dose-dependent mechanism); (3) interstitial nephritis induced by drugs and their metabolites (a dose-independent mechanism).…”

Section: The Mechanism Of Kidney Injuries Induced By Drugs and Their Metabolitesmentioning

confidence: 99%

The Mechanism of Drug Nephrotoxicity and the Methods for Preventing Kidney Damage

Kwiatkowska

Domański

Dziedziejko

et al. 2021

IJMS

111

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Acute kidney injury (AKI) is a global health challenge of vast proportions, as approx. 13.3% of people worldwide are affected annually. The pathophysiology of AKI is very complex, but its main causes are sepsis, ischemia, and nephrotoxicity. Nephrotoxicity is mainly associated with the use of drugs. Drug-induced AKI accounts for 19–26% of all hospitalized cases. Drug-induced nephrotoxicity develops according to one of the three mechanisms: (1) proximal tubular injury and acute tubular necrosis (ATN) (a dose-dependent mechanism), where the cause is related to apical contact with drugs or their metabolites, the transport of drugs and their metabolites from the apical surface, and the secretion of drugs from the basolateral surface into the tubular lumen; (2) tubular obstruction by crystals or casts containing drugs and their metabolites (a dose-dependent mechanism); (3) interstitial nephritis induced by drugs and their metabolites (a dose-independent mechanism). In this article, the mechanisms of the individual types of injury will be described. Specific groups of drugs will be linked to specific injuries. Additionally, the risk factors for the development of AKI and the methods for preventing and/or treating the condition will be discussed.

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“…In addition, drugs may precipitate, crystallize, or create casts in the distal tubules, resulting in tubular blockage (Luque et al 2017). Another pathway involves interstitial tubule inflammation, which causes interstitial nephritis (Chamarthi et al 2018). Therefore, drug-induced nephrotoxicity occurs through one of the three routes mentioned (Zuk and Bonventre 2016).…”

Section: Introductionmentioning

confidence: 99%

Anti-nephrotoxic activity of aqueous extract of polyherbal mixture against renal toxicity induced by paracetamol in Wistar albino rats

ABU

Mashi²,

Lawal³

et al. 2023

Nusantara Biosci

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Abstract. Abu MS, Mashi RL, Lawal JY, Samuel OS. 2023. Anti-nephrotoxic activity of aqueous extract of polyherbal mixture against renal toxicity induced by paracetamol in Wistar albino rats. Nusantara Bioscience 15: 112-117. Medicinal plant materials as sources of therapeutic compounds continue to play an important role in maintaining human health for ages. This study investigated the effect of polyherbal extract (Carica papaya L., Allium sativum L., Curcuma longa L., and Azadirachta indica A.Juss.) on urea, creatinine, sodium ion, potassium ion, and chloride ion concentrations, and body weight of Wistar rats intoxicated with paracetamol. Thirty Wistar rats were randomly distributed into six groups, with five in each group. Group 1 is the normal control group; Group 2 is the negative control group (paracetamol-induced but untreated); Group 3 received 140 mgkg-1 of silymarin; Groups 4, 5, and 6 received 100, 300, and 500 mgkg-1 body of the aqueous polyherbal extract respectively for seven days. Therefore, the blood samples were collected and evaluated for creatinine, urea, sodium, potassium, and chloride ions concentrations to measure kidney function. The results revealed that the aqueous extract of the polyherbal mixture significantly (p<0.05) ameliorated the kidney function test parameters that were analyzed by lowering their concentrations previously elevated by the paracetamol intoxication comparable with the normal control rats. Therefore, it can be concluded that the polyherbal mixture extract expressed an anti-nephrotoxic effect against renal toxicity induced by paracetamol in Wistar albino rats.

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Acute interstitial nephritis: a multifaceted disease

Cited by 6 publications

References 6 publications

Severe acute interstitial nephritis induced by valsartan

Severe acute interstitial nephritis induced by valsartan

The Mechanism of Drug Nephrotoxicity and the Methods for Preventing Kidney Damage

Anti-nephrotoxic activity of aqueous extract of polyherbal mixture against renal toxicity induced by paracetamol in Wistar albino rats

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