75 year old male with metastatic myeloma presenting with AMS , polyuria and neutropenic fever.

By MedCase Editor - MD | Dec 5, 2019

75-year-old gentleman past medical history significant for DM TYPE 2, recent diagnosis of multiple myeloma. He was started on chemotherapy with CyBorD regimen. On admission to the hospital he was noticed to have complains of fever temperature of 101.5 degrees Fahrenheit, leukocytosis, chills,. He was started on empiric IV antibiotic therapy with cefepime n. His absolute neutrophil count was 232 /microL. . Patient continued to persistent fever on day 5.. patient was started on non-liposomal preparation of amphotericin B.

Vital signs showed blood pressure 125/78, respiration of 16 pulse 75
on exam he was drowsy with AMS barely arousable. MRI brain shows revealed a 3.1 X 2.6 X 3.6 cm lobulated mass in left lateral ventricle trigone

Lab results reviewed showed
Sodium 155, chloride 124, potassium 3.5, magnesium 1.6 BUN 125, creation 4.4, bicarbonate of 16, calcium 11.2
PTH 45 pg/mL
24-hour urine potassium was 45 mEq/day
24-hour urine magnesium was 85 mg/day
Urine osmolality 150 mOsm/L
Urine output in 24 hours 5 L/day

Following a desmopressin challenge as per standard protocols, a dose of 10 μg of desmopressin was administered intranasally thrice daily. Subsequently, the patient’s blood serum sodium levels gradually fell from 155 mEq/L to 153 mEq/. His urinary output decreased to 4.5 L/day and then 4.3 L/day, respectively after the administration of desmopressin.

Which is the most likely reason for patients polyuria ?

Explanation:

A. Patient most likely has amphotericin B induced nephrotoxicity due to use of nonliposomal preparation. Amphotericin can cause acute kidney injury both due to direct toxic effect on renal tubules and also also from renal vasoconstriction due to direct effect of amphotericin B on renal vasculature and from acute tubular glomerular feedback mediated by increased sodium entry into juxtaglomerular cells mediated by increased ion permeability induced by enhanced membrane permeability due to Amphotericin.

Amphotericin also causes increased urinary potassium wasting, hypokalemia, increased urinary magnesium wasting and low serum magnesium levels, type 1, distal RTA. It also causes polyuria due to to nephrogenic diabetes by increasing resistance to ADH hormone. Hypokalemia induced by amphotericin can also cause nephrogenic diabetes insipidus by causing adh hormone resistance

 

B. B. Osmolar diuresis from high BUN is associated with increased urine osmolality. However patient urine osmolality is low in the 100 mOsm/L range and does not explain polyuria. He also has acute kidney injury decreasing glomerular filtration making it less likely to have polyuria.

C. Metastatic CNS-posterior pituitary lesions from myeloma can cause central diabetes insipidus.MRI of the brain revealed a 3.1 X 2.6 X 3.6 cm lobulated mass in left lateral ventricle trigone Which is not associated with ADH deficiency. Lack of response to desmopressin challenge also makes central diabetes insipidus less likely.

D. Patient’s hypercalcemia is very mild and does not explain this to polyuria. Hypercalcemia can cause decreased sodium chloride reabsorption in the ascending limb of the renal tubules decrease in medullary osmotic gradient making ADH hormone ineffective.

 

 

 

Case reviewed by MedCase Editor

Designation: MD

ABIM Board Certified Nephrology

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