An Unusual Case of Nephrotic Syndrome Preceded by Chronic Mercury Poisoning

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ESPR424
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History: A 7 year old boy presented to ED upon referral from PMD for 1 week of generalized edema and 3.5kg weight gain in 24 hour period. Further history revealed recurrent episodic swelling over the last year, including additional episodes attributed to allergies and treated with steroids. Three years prior, he had presented to several healthcare providers with a constellation of unexplained signs and symptoms including diaphoresis, headache, tactile sensitivity, decreased appetite, and insomnia within a month of moving into a new home with his family. Initial laboratory evaluation was unrevealing but a 24-hour urine assay for heavy metals was significant for a urine mercury concentration of 52 mcg/L (nml range <10 mcg/L). The patient's siblings and parents were also tested and noted to have elevated 24-hour urine mercury concentrations. The local health department detected the presence of elevated mercury concentrations within the home. The family was treated with chelation therapy dimercaptosuccinic acid with resolution of symptoms and 24-hour urine mercury concentrations to baseline by six months. The source of the mercury exposure was traced back to the previous homeowner, who had spilled elemental mercury, which had entered the home's heating, ventilation, and air conditioning (HVAC) system, leading to inhalational mercury vapor exposure for the entire family.

 Physical Exam/Labs:

PE: VS: HR 99, BP 140/80, RR 25, SpO2 98%, Temp 98.5, Wt 25.5kg

 GENERAL - alert, well appearing, and in no acute distress; diffusely edematous with puffy face
 HENT - NCAT, nose is normal and patent with no erythema or discharge, MMM, pharynx normal without lesions; face edematous compared to baseline photographs
 EYES -  PERRL, EOMI, no conjunctival icterus or injection, no discharge  
 NECK - supple, no cervical lymphadenopathy
 CHEST - comfortable RR. Good, equal air entry bilaterally. No retractions. CTAB, no w/r/r
 HEART - RRR, normal S1, S2, no murmurs, 2+ pulses bilaterally, capillary refill <2 seconds
 ABDOMEN - +BS, soft, non-tender, diffusely enlarged, no masses or organomegaly
 GU- normal penis with scrotal edema
 NEURO - alert, MAEE by observation, age appropriate behavior, symmetric facial movements, follows commands
 EXTR - WWP, peripheral pulses 2+, cap refill <2 sec, pitting edema bilateral legs to knee
 SKIN - R axillary rash


Urinalysis: SG >1.035, pH 6.0, leuk esterase neg, nitrate neg, protein >300, glucose neg, blood neg, yeast rare

CBC: WBC 14.45, Hgb 13.7, Hct 39.1, Plt 618

Renal Function Panel: Na 133, K 5.8, Cl 106, CO2 19, BUN 35, Cr 0.4, Ca 7.2, Alb 0.7, Phos 6.1

Lipids: Total Cholesterol 457 mg/dL

Urine protein/creatinine ratio: 9.8 mg/mg (nml <0.2)

C3 139 mg/dL (nml 80-170 mg/dL), C4 16.4 mg/dL (nml 14-44 mg/dL), ASO <50.0 (nml 0-200)

Urine Mercury, Random: non-detected
Blood Mercury: <4 (Nml <=10)

Diagnosis/Discussion:  This case describes an unusual presentation of delayed nephrotic syndrome following mercury exposure and successful chelation treatment in a young boy. Following presentation to the Emergency Department, the patient was admitted to the Nephrology service and received three rounds of forced diuresis with 25% albumin infusion and 1mg/kg furosemide. He was initiated on prednisone 1mg/kg twice daily for treatment and famotidine for gastric prophylaxis. Prior to discharge, his anasarca improved and proteinuria resolved within one week of discharge. He achieved sustained remission after completing a 12 week course of steroids according to the Mendoza Protocol.
Mercury-induced nephropathy is generally diagnosed during the acute phase of illness after mercury exposure and delayed presentations are very rare. In the case described here, the lengthy duration of time between the patient's mercury exposure and his diagnosis of NS suggests that the nephropathy was not a direct sequelae of elemental mercury vapor exposure but could be a contributing factor. The pathophysiology of mercury-induced nephropathy is not well understood, but may be related to idiosyncratic reactions or immune-mediated effects of mercury on the kidneys. Although these findings suggest that heavy metal exposure may result in immunologic kidney diseases, genetic factors likely also influence the incidence and penetrance of this condition, and may help explain why the patient in the case described herein developed NS but his siblings who sustained mercury intoxication did have any sequelae. Due to the uncommon incidence of NS in the pediatric population as well as the frequently idiopathic nature of this condition, a direct causation between the diagnosis of NS and a prior history of mercury intoxication can be challenging to establish.

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INOVA Children's Hospital
Inova Childrens Hospital
Inova Children's Hospital

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