Drug-Induced Hypersensitivity Nephritis: Lymphocyte Stimulation Testing and Renal Biopsy in 10 Cases

Joh, Keiichiro; Aizawa, Shigeo; Yamaguchi, Y; Inomata, Izuru; Shibasaki, Toshiaki; Sakai, O; Hamaguchi, K

doi:10.1159/000168085

Cited by 36 publications

(20 citation statements)

References 20 publications

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“…Although the usefulness of LST and renal biopsy has been reported in the diagnosis of drug-induced tubulointerstitial nephritis, 12 positive results for these examinations were not obtained in our patient. Concerning LST, a positive result is not always obtained in the diagnosis of drug-induced tubulointerstitial lesions.…”

Section: Discussioncontrasting

confidence: 73%

Distal type of renal tubular acidosis after anti-epileptic therapy in a girl with infantile spasms

Tanaka¹,

Onodera²,

Ito³

et al. 1999

Clinical and Experimental Nephrology

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distal type renal tubular acidosis (RTA) associated with VPA therapy has not been reported previously. We encountered a girl with infantile spasms (West syndrome). VPA administration had proven to be of benefit in her infantlie spasms; however, she subsequently developed distal type RTA combined with a mild bicarbonate wasting after 4-month VPA administration. Although a percutaneous renal biopsy failed to show tubulointerstitial lesions, her clinical course indicated that the RTA was probably caused by VPA administration. Case reportThe patient was 11 months old at presentation. She was born at 39 weeks gestation after an uncomplicated pregnancy, with a birth weight of 3774 g. No perinatal events were documented, and her early development was normal. At 6 months she experienced the first episode of tonic spasms. Laboratory findings and a findings in a search for intracranial lesions by magnetic resonance imaging were unremarkable. There was no acidosis. Electroencephalography (EEG) showed typical hypsarrhythmia. Ophthalmological examination revealed no abnormalities. She was diagnosed as having West syndrome, and a 2-week course of intramuscular thyrotropin-releasing hormone (TRH, 0.5 mg per day), followed by a 2-week course of adrenocorticotropic hormone (ACTH; 0.01 mg/kg per day) combined with oral VPA (30 mg/kg per day) and vitamin B6 therapy was commenced at the age of 7 months. After cessation of ACTH, administration of VPA (20 mg/kg per day) with vitamin B6 was continued. Thereafter, the therapy proved to be of benefit in her infantile spasms, with a gradual subsidence of tonic spasms and EEG abnormalities. Developmental delay was not observed. The serum VPA level ranged from 45 to 71 µg/ml (therapeutic range, 50-100 µg/ml).At 11 months she was admitted to our hospital because of nausea, vomiting, and poor physical activity without any seizures. Physical examination revealed a moderately deAbstract An 11-month-old girl was referred to our hospital because of nausea and poor physical activity. She had a 5-month history of infantile spasms, which were successfully treated with valproic acid (VPA) and vitamin B6. Laboratory studies revealed hyperchloremic metabolic acidosis, mainly due to distal type renal tubular acidosis (RTA). Although a renal biopsy, performed 2 months after the onset of RTA, did not demonstrate tubulointerstitial lesions, her clinical course, in which administration of VPA led to an episode of RTA, with gradual subsidence on VPA removal, suggested that the probable causative agent of her distal type RTA was VPA. Although proximal type RTA associated with VPA administration has been reported, distal type is rarely seen. To our knowledge, a similar case has not been reported previously.

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Section: Discussioncontrasting

confidence: 73%

Distal type of renal tubular acidosis after anti-epileptic therapy in a girl with infantile spasms

Tanaka¹,

Onodera²,

Ito³

et al. 1999

Clinical and Experimental Nephrology

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“…Other drug-related abnormalities may be found concomitantly, such as haemolytic anaemia and liver injury. Elevation of total IgE has been found in about 50% of cases [42]. Immunological investigation with antibodies against deoxyribonucleic acid and anti-nuclear and serum complement are usually normal, except in rare auto-immune disease, such as lupus interstitial nephritis [36,43].…”

Section: Clinical Presentationmentioning

confidence: 99%

Acute tubulointerstitial nephritis

et al. 2011

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Acute tubulointerstitial nephritis (TIN) is a frequent cause of acute renal failure, characterised by the presence of inflammatory cell infiltrate in the interstitium of the kidney. Immuno-allergic reaction to certain medications, mainly non-steroidal anti-inflammatory drugs and antibiotics are by far the most important etiology for TIN today, but other situations such as infections, toxins, and vasculitis are known to induce TIN. Incidence of TIN is increasing, probably due to prescription habits and NSAID overuse, representing 3-7% of acute kidney injury in biopsies in children. Avoidance of the causal substance and rapid steroid therapy are hallmarks for patient care, but spontaneous initial recovery is very frequent and the general prognosis seems satisfactory. However, development of chronic TIN, without response to steroid or other immunosuppressive treatment, is possible. As the largest part of TIN is secondary to certain drugs, clear indications in particular for NSAID or antibiotics should be respected to reduce the number of TIN cases.

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“…A set of seven case series compared AIN treated with corticosteroids (52 patients) and without corticosteroids (48 patients) . Persistent renal dysfunction (S cr higher than 2.3 mg/dl) occurred in 17% of those treated with corticosteroids compared with 19% of those treated without corticosteroids (p value not reported).…”

Section: Discussionmentioning

confidence: 99%

Azithromycin‐Induced, Biopsy‐Proven Acute Interstitial Nephritis in an Adult Successfully Treated with Low‐Dose Corticosteroids

et al. 2015

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Acute interstitial nephritis (AIN) is a form of acute kidney injury (AKI) characterized by a rapid deterioration of renal function, inflammatory infiltration of interstitial tissues, and renal edema. Drug-induced AIN is the most common etiology of AIN, but AIN can also have infectious, autoimmune, or idiopathic causes. β-Lactam antibacterials, nonsteroidal antiinflammatory drugs, and proton pump inhibitors are recognized as leading causes of AIN; however, many other drugs have been identified as causes. We describe the case of a 59-year-old white male who developed AIN that required hemodialysis following azithromycin treatment. He presented to the hospital with complaints of nausea, vomiting, malaise, and fever over the past 3 days, along with no urine output in the preceding 24 hours. Two weeks earlier, he had completed a 5-day course of azithromycin 500 mg on day 1 followed by 250 mg/day on days 2-5 (total dose 1.5 g) for an upper respiratory tract infection. On admission, the patient's serum creatinine (S(cr)) concentration was 7.4 mg/dl (baseline = 1.3 mg/dl). He reported a similar episode of kidney failure 2 years earlier after taking azithromycin; however, at that time it was believed the AKI was likely due to benazepril use in the setting of acute infection, and a kidney biopsy was not performed. His S(cr) concentration peaked at 11.4 mg/dl, and three sessions of hemodialysis were required. A kidney biopsy was performed that revealed AIN. Low-dose prednisone 0.3 mg/kg (30 mg)/day, tapered over the next 3 months, was administered, and his renal function improved to near baseline prior to discharge; 6 months later, his Scr concentration was 1.4 mg/dl. Despite lower than recommended dosing, this patient responded well to prednisone and did not experience long-term sequelae from renal injury. Use of the Naranjo Adverse Drug Reaction Probability Scale indicated a definite relationship (score of 10) between azithromycin exposure and the manifestation of AIN. To our knowledge, this is the first report of azithromycin-induced acute interstitial nephritis with near-complete resolution of renal injury in an adult. This case report illustrates the importance of rapid recognition of drug-induced renal injuries and discontinuation of the offending agent. Select use of corticosteroids may improve both time to and extent of renal function recovery.

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Drug-Induced Hypersensitivity Nephritis: Lymphocyte Stimulation Testing and Renal Biopsy in 10 Cases

Cited by 36 publications

References 20 publications

Distal type of renal tubular acidosis after anti-epileptic therapy in a girl with infantile spasms

Distal type of renal tubular acidosis after anti-epileptic therapy in a girl with infantile spasms

Acute tubulointerstitial nephritis

Azithromycin‐Induced, Biopsy‐Proven Acute Interstitial Nephritis in an Adult Successfully Treated with Low‐Dose Corticosteroids

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