Interstitial Nephritis Caused by Trimethoprim-Sulfamethoxazole in Renal Transplant Recipients

Underlying renal insufficiency: the pivotal risk factor for Pneumocystis jirovecii pneumonia in immunosuppressed patients with non-transplant glomerular disease

“…The maximum serum concentrations of TMP and SMX after 3 days of administration have been shown to be 13.6 ± 2.0 and 372 ± 64 μg/mL, respectively, in healthy adults receiving the conventional doses of 20 mg/kg/day TMP and 100 mg/kg/day SMX for PCP [33]. The mechanism of AKI development during TMP-SMX treatment has been reported to involve crystal formation, interstitial nephritis and acute tubular necrosis [34,35]. In our study, renal impairment was transient, and nearly all cases of AKI resolved promptly after the discontinuation of therapy in surviving patients; therefore, crystal formation, rather than interstitial nephritis, was likely responsible for the majority of cases in our study.…”

Severe Hyponatremia and Hyperkalemia Induced by Trimethoprim-Sulfamethoxazole in Patients with Pneumocystis carinii Pneumonia.

“…This drug is excreted from the kidney and is known to have side effects such as acute tubular necrosis and interstitial nephritis (1)(2)(3). Tmp-Smxhas been reported to cause renal salt wasting and metabolic acidosis (4), but appears to have no remarkableeffects on serum electrolyte levels as long as regular-dose Tmp-Smx is administered (5).…”

Acute Granulomatous Interstitial Nephritis Due to Co-Trimoxazole

“…Sulfonamide had previously been associated with renal granulomas by More et al [14], who described 8 cases in a series of 375 autopsies of patients treated with this drug. The granulomatous response in AIN is believed to be an immunologic response to the drug and not a direct response to crystalline deposition in the interstitium [15,16]. Three immunologic mechanisms for this lesion have been proposed, including production of antitubular basement membrane antibodies, cell-me diated hypersensitivity, and deposition of circulating complexes of IgG or complement [3,17], The clinical features of AIN due to co-trimoxazole are usually far more subtle than the case we have described.…”

“…As others have suggested [ 15], it is likely that the presence of underlying renal disease and hypertension were contributory factors in precipitating the severe but reversible insult. Co-trimoxazole-induced AIN has also been described in renal transplant recipi ents who are commonly on multiple medications and immunosuppressive regimens [16,18]. In this situation the biopsy pattern can be confusing, and the clinical interpretation is further complicated by the well-known effect of trimethoprim in interfering with the tubular secretion of creatinine, raising the serum creatinine lev el, and resulting in a lower creatinine clearance without actually effecting renal function [19].…”

“…In this situation the biopsy pattern can be confusing, and the clinical interpretation is further complicated by the well-known effect of trimethoprim in interfering with the tubular secretion of creatinine, raising the serum creatinine lev el, and resulting in a lower creatinine clearance without actually effecting renal function [19]. Eosinophilia is felt to be helpful in pointing toward drug hypersensitivity, but caution has been advised in using this drug in the transplant setting [16].…”