Sulfadiazine crystalluria revisited. The treatment of Toxoplasma encephalitis in patients with acquired immunodeficiency syndrome

Simon, Daniel I.; Brosius, Frank C.; Rothstein, David M.

doi:10.1001/archinte.150.11.2379

Cited by 31 publications

(39 citation statements)

References 25 publications

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“…Use of high-dose sulfadiazine can, on rare occasions, also cause crystal nephropathy. 38,39 Urine microscopy in this case may reveal the characteristic birefringent, needle-shaped crystals arranged in a "shocks of wheat" pattern. Crystal precipitation typically occurs in acidic urine and in low-flow states.…”

Section: Antimicrobial Agents Aminoglycosidesmentioning

confidence: 86%

Drug-induced impairment of renal function

Pazhayattil¹,

Shirali²

2014

IJNRD

117

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Pharmaceutical agents provide diagnostic and therapeutic utility that are central to patient care. However, all agents also carry adverse drug effect profiles. While most of these are clinically insignificant, some drugs may cause unacceptable toxicity that impacts negatively on patient morbidity and mortality. Recognizing adverse effects is important for administering appropriate drug doses, instituting preventive strategies, and withdrawing the offending agent due to toxicity. In the present article, we will review those drugs that are associated with impaired renal function. By focusing on pharmaceutical agents that are currently in clinical practice, we will provide an overview of nephrotoxic drugs that a treating physician is most likely to encounter. In doing so, we will summarize risk factors for nephrotoxicity, describe clinical manifestations, and address preventive and treatment strategies.

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Section: Antimicrobial Agents Aminoglycosidesmentioning

confidence: 86%

Drug-induced impairment of renal function

Pazhayattil¹,

Shirali²

2014

IJNRD

117

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“…The onset of parasitosis-associated nephropathy has been reported in cases of malaria, schistosomiasis, toxoplasmosis, syphilis, and other infections [16][17][18], but very few reports of nephropathy associated with S. stercoralis infection are available. Only 16 such cases, including the present case, have been reported to date (Table 2), and 15 of the patients developed nephrotic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Minimal change nephrotic syndrome in a patient with strongyloidiasis

et al. 2010

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Strongyloidiasis, a chronic infection caused by the intestinal parasite Strongyloides stercoralis, is prevalent in the Nansei Islands of Japan. Here, we report our findings on a case of strongyloidiasis complicated with steroid-resistant minimal change nephrotic syndrome in a 69-year-old male resident of Fukuoka Prefecture who had lived in Yakushima, one of the Nansei Islands, until age 15. In October 2006, he developed proteinuria and edema, and was diagnosed with minimal change nephrotic syndrome on the basis of the renal biopsy findings. Following treatment with prednisolone, the level of proteinuria decreased to 0.29 g/day by day 35. However, 5 days later (day 40), the patient developed persistent watery diarrhea and vomiting, leading to dehydration and malnutrition. Pneumonia and bacterial meningitis subsequently developed (day 146); filarial (infectious-type) and rhabditiform (noninfectious-type) S. stercoralis larvae were detected for the first time in the patient's sputum, gastric juice, feces, and urine. Although treatment with ivermectin was started immediately and the parasitosis responded to the treatment, the patient died of sepsis. Consequently, although strongyloidiasis is a rare infection except in endemic regions, it is essential to consider the possibility of this disease and begin treatment early for patients who have lived in endemic areas and who complain of unexplained diarrhea during steroid-induced or other immunosuppression.

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“…1 With the relatively recent increased use of sulfadiazine to treat toxoplasmosis, sulfadiazine-induced crystal nephropathy has re-emerged as a clinical entity.…”

Section: Discussionmentioning

confidence: 99%

Sulfadiazine‐induced crystal nephropathy: a new ‘old’ problem

et al. 2015

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With a greater awareness of toxoplasmosis infections, and increased prescribing of sulfadaizine, it is timely to remind colleagues of a largely forgotten clinical presentation. We present the case of crystal nephropathy secondary to sulfadiazine prescribed for retinal toxoplasmosis.A 60 year-old with left chorioretinal toxoplasmosis presented with 18 h of severe bilateral constant flank pain, nausea and acute kidney injury. He had no known renal disease. He had normal renal function prior to commencement of pyrimethamine 75 mg and sulfadiazine 1.5 g four times daily 6 days earlier.He was afebrile, blood pressure was 163/99 mmHg, and his abdominal examination revealed marked bilateral renal angle tenderness. His urine output was reduced. Initial plasma creatinine was 309 umol/L, and peaked at 530 umol/L, before rapidly improving following intervention. Urine microscopy showed many crystals, including dumbbell-shaped crystals ( Fig. 1) with a positive Lignin test. Urinalysis showed no haematuria or proteinuria, pH 6 and <10 × 10 6 white cells/L. These urinary findings confirmed a diagnosis of sulfadiazine-induced crystal nephropathy.The patient was treated with intravenous sodium bicarbonate, 0.9% saline and frusemide to achieve a urine output over 100 mL/h and urine pH above 7.15. Following 3 days of treatment, the urine was devoid of crystals, and the lignin test was now negative, indicating resolving sulfadiazineinduced crystal nephropathy. One week later, his renal function had returned to normal. DISCUSSIONSulfadiazine was well known to induce a crystal nephropathy in the two decades after it was introduced in 1936 before the availability of more water-soluble sulphonamides.1 With the relatively recent increased use of sulfadiazine to treat toxoplasmosis, sulfadiazine-induced crystal nephropathy has re-emerged as a clinical entity.Known predisposing factors to favour crystal deposition include volume depletion, hypoalbuminaemia, chronic kidney disease and inadequate dose adjustment, thereby increasing the urinary sulfadiazine concentration. A persistent acidic urinary pH (pH < 5.5) increases the likelihood of crystal deposition in the renal tubules.1 Urinary sediment examination reveals crystals typically shaped of needles, rosettes or 'shocks of wheat'. 2Treatment involves cessation of sulfadiazine, aggressive volume repletion and urine alkalization to target a urinary pH of >7.15.1 Prognosis in sulfadiazine-induced crystal nephropathy is favourable, with renal recovery over a mean of 8.3 days.3 Recommencement of sulfadiazine therapy is not contraindicated provided there is a high urine flow rate and urine alkalinization (pH >7.15) with monitoring of renal function and urinalysis for crystals.

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Sulfadiazine crystalluria revisited. The treatment of Toxoplasma encephalitis in patients with acquired immunodeficiency syndrome

Cited by 31 publications

References 25 publications

Drug-induced impairment of renal function

Drug-induced impairment of renal function

Minimal change nephrotic syndrome in a patient with strongyloidiasis

Sulfadiazine‐induced crystal nephropathy: a new ‘old’ problem

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