∣ A Caucasian male with dark skin, black urine, and acute kidney injury Overview

  • Presenting Complaint
  • Patient History
  • Review of Systems
  • Physical Examination
  • Diagnostic Test
  • Diagnostic Imaging
  • Diagnosis and Management
  • Discussion

A 38-year-old Caucasian male was admitted for onset of ascites, oliguria, acute kidney injury (AKI), and black urine.

  • History of presenting
  • Past Medical/Social history
  • Past surgical history
  • Family history
  • Current Medication
A 38-year-old Caucasian male was admitted for onset of ascites. An abdominal computed tomography scan showed multiple hypodense lesions in the liver (Figure 1). An uncomplicated paracentesis was carried out on the second hospital day. The serum-ascites albumin gradient of 1.5 g/dl was suggestive of portal hypertension. A week later, a renal consultation was requested for oliguria, acute kidney injury (AKI), and black urine, which the patient had noted first in the 2 weeks before admission. There had been no episodes of hypotension, no exposure to nephrotoxic agents, and no evidence of sepsis to explain the AKI.
black urine
ascites

General

Normocephalic, conjunctivae/corneas clear. PERRL, EOM's intact.Septum midline. Mucosa normal. No drainage or sinus tenderness.

Heent

no thyromegaly, conjunctiva normal , normal dentition, no JVD

Neck

no carotid bruits, trachea midline, no lymphadenopathy,

Cardiovascular

RRR, no murmur or extra heart sounds auscultated.

Lungs

CTAB, no respiratory distress or retractions. No wheezing.

Abdomen

Soft, Non tender on palpation ,ASCITES, normal BS, no hepatosplenomegaly. No rebound

Extremities

extremities normal, atraumatic, no cyanosis or edema, pulses positive and symmetric

Skin

normal turgor, no rashes,

Neurological Exam

no focal neurological deficits, normal power, sensations normal. reflex within normal range
  • Bio Chemistry
  • Pathology
  • Microbiology
  • Hematology
  • Miscellaneous

Sodium: 132 meq/L( normal 135-145 meq/L)

Potassium: 5.6 meq/L (normal 3.5-5.0 meq/L)

Chloride: 98 meq/L(normal 96-108 meq/L)

Bicarb: 18 meq/L(normal 22-30 meq/L)

Magnesium: 1.7 mg/dl ( normal 1.7 to 2.2 mg/dL )

Phos.: WNL mg/dl ( normal 2.8 to 4.5 mg/dL)

Bun: 33 mg/dl ( normal 6-23 mg/dL)

Creat: 1.8 mg/dl ( normal 0.7 -1.3 mg/dL)

Liver Enzymes - SGOT/AST: WNL U/L ( normal 1-35 )

SGPT/ ALT: WNL U/L ( normal 1-45 )

GGT: WNL U/L ( normal 8-38 )

Direct Bilirubin: WNL mg/dl ( normal 0.1-0.3 )

Total Bilirubin: WNL mg/dl ( normal 0.1 - 1.2 )

ALBUMIN: 2.7

URINE : His urine appeared black without clumps of tissue or blood clots (Figure 2). Urine dipstick could not be read because of an interfering substance. The spot urine sodium was <10 mmol/l.

Hemoglobin: WNL g/dl ( normal 13.9 -16.3)

Hematocrit: WNL % ( normal 42-52 % )

White Count: WNL ( normal 4,500 to 11,000 WBCs per microliter)

Platelets: WNL ( normal 150,000 to 450,000 platelets per microliter)

Differential: WNL

  • CT Scan
  • Xray
  • MRI
  • Ultrasound
  • Echo
  • Endoscopic
  • Miscellaneous

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Melanuria is present in approximately 15% of cases with metastatic disease.

It is caused by the excretion of a chromogen (5:6 dihydroxy-indole) in the urine, which is an intermediate product of the production of melanin from tyrosine.

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It is hypothesized that larger pigment emboli are deposited within the glomeruli, allowing larger melanin granules to pass through the damaged filtration barrier and making the urine dark on voiding.

Histopathologic evidence of glomerular pigment emboli was present in a case report, but renal function remained normal in that patient.

A single case of AKI caused by melanin accumulation within the tubular lumen, tubular cells, and endothelial cells of the vessels and glomeruli has been reported.

Our patient also had urinary findings suggestive of acute tubular necrosis, but brown pigmented tubular casts can also be seen in patients with melanuria alone. The cause of his AKI was most likely a hepatorenal-like syndrome, suggested by the absence of protein, red and white cells in the urine, low urine sodium, and no improvement of renal function with volume expansion.

Case reviewed by MEDCASE EDITOR

Designation: MD

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