Sir,A seven-year-old female presented with puffiness of eyes, headache, and oliguria since two days. There was no fever, convulsion, altered sensorium, visual disturbances, recent sore throat infection, or pyoderma. She had varicella two weeks prior to admission. On admission, she was afebrile with a heart rate of 102/min, respiratory rate of 24/min, and blood pressure of 150/100 mmHg (>95th percentile for age and sex). Post-varicella rash was present on the body. There was periorbital puffiness and mild edema of feet. Respiratory system examination revealed reduced air entry in the inframammary and infra-axillary region bilaterally. Shifting dullness was present on abdominal examination. Liver was nontender with a span of 7.5 cm. Rest of the examination was normal. Investigations revealed: Hemoglobin, 10.2 gm/dl; total leukocyte count, 7600/cumm; and platelet count, 3.2 lac/cumm. Erythrocyte sedimentation rate was 56 mm at the end of one hour. Urine microscopy revealed 20 red blood cell/hpf and red blood cell casts. Renal function test, liver functions test, serum electrolytes, and throat swab culture were normal. Antistreptolysin-O and antideoxyribonuclease-B titer were negative. Ultrasonography of abdomen revealed bilateral mild pleural effusion and ascitis with grade 1 altered echogenicity of both the kidneys. Serum complement was 20 (80-200 mg/dl). Oral furosemide and nifedipine was started. Urine output became normal on the third day. She was discharged after four days. Antihypertensives were gradually tapered and omitted after four weeks. Urinalysis and serum complement level after eight weeks were normal.The association of nephritis with varicella was first described by Henoch in 1884.[1] Renal involvement in varicella is rare with an incidence of 0.12 to 19%.[12] Various temporal relationships between varicella and the presentation of renal disease have been described. Glomerulonephritis can develop after a latent period of 7 to 14 days or can develop either prior to or with the appearance of varicella rash.[13] The course is usually benign with a complete recovery. Glomerulonephritis due to varicella generally resembles post-streptococcal glomerulonephritis (commonest cause of glomerulonephritis in children), excluding its initial stage, i.e., glomerulonephritis with varicella can start after a latent period, before, or concomitantly with the infection. The precise mechanism of varicella-induced glomerulonephritis is not known. Both direct damage and immune-mediated damage have been proposed.[12] Clinical and histological evidence suggests that viruria resulting from active infection of kidney cells can cause renal damage in varicella.[1] Glomerulonephritis either prior to or with the appearance of the varicella rash occurs by this mechanism. Such unusual presentations can result in diagnostic dilemma.[4] On the contrary, the characteristic latent period and depression of serum complement activity suggests that glomerulonephritis in our patient was due to immune-mediated damage. Other types of renal involvement in varicella include post-streptococcal glomerulonephritis flare-up in a patient with varicella, glomerulonephritis associated with varicella and streptococcal infection, rapidly progressive glomerulonephritis, and nephrotic syndrome following varicella.[15]