To the Editor:
We report 2 transient renal tubular syndromes associated with coronavirus disease 2019 (COVID-19).
A 47-year-old patient in a neurorehabilitation unit was diagnosed with COVID-19 following onset of respiratory symptoms and pyrexia, confirmed by reverse transcriptase polymerase chain reaction. Ten days later, he developed hypernatremia with an acute kidney injury. He was exclusively fed by percutaneous endoscopic gastrostomy tube.
Investigations (Table 1) supported a diagnosis of nephrogenic diabetes insipidus. He was managed with increased enteral water intake via the percutaneous endoscopic gastrostomy and intravenous 5% dextrose over 24 hours. Biochemistry improved progressively, with serum sodium renal function returning to baseline by day 23.
Table 1.
Serum and urine biochemistry
| Patient 1 | Patient 2 | |
|---|---|---|
| Age, yr | 47 | 52 |
| Gender | Male | Female |
| Past medical history | Traumatic head injury 2018, PEG-fed | Diabetic nephropathy, kidney/pancreas transplant 2011 |
| Drug therapy | Meropenem | Tacrolimus, mycophenolate (suspended), meropenem |
| Date of COVID-19 diagnosis | April 3, 2020 | March 26, 2020 |
| Onset of syndrome, days after COVID diagnosis | 10 | 3 |
| Resolution of syndrome, d | 21 | 18 |
| Serum sodium, mmol/l | 152 | 138 |
| Serum potassium, mmol/l | 3.6 | 2.9 |
| Serum creatinine, μmol/l | 154 | 90 |
| Baseline serum creatinine, μmol/l | 60 | 62 |
| Serum bicarbonate, mmol/l | 30 | 4 |
| Serum corrected calcium, mmol/l | 2.56 | 2.41 |
| Serum phosphate, mmol/l | 1.83 | 0.18 |
| Serum magnesium, mmol/l | 1.03 | 0.56 |
| Serum osmolality, mosmol/l | 321 | ND |
| CRP, mg/l | 74 | 100 |
| Urinary FEPO4, % | ND | 70 |
| Urinary retinol binding protein/creatinine ratio | ND | 1540 |
| Urinary osmolality, mosmol/l | 264 | ND |
CRP, C-reactive protein; ND, not done; PEG, percutaneous endoscopic gastrostomy.
A 52-year-old woman with diabetic nephropathy and a kidney-pancreas transplant was recovering from a below-knee amputation. She developed fever and a cough; reverse transcriptase polymerase chain reaction confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Three days later, she developed a severe metabolic acidosis associated with profound hypophosphatemia, hyperphosphaturia, and low molecular weight proteinuria, diagnostic of the renal Fanconi syndrome (Table 1). She required aggressive i.v. potassium, bicarbonate, and phosphate supplementation; she was weaned off all supplementation by day 18.
Kidney disease is widely recognized in COVID-19; there is evidence of direct viral invasion of the tubular epithelium.1,2 Angiotensin-converting enzyme 2 (ACE2), the ligand for viral cell invasion, is expressed on both proximal and distal tubular cells.3 The first patient had a distal lesion (nephrogenic diabetes insipidus); the second had proximal tubular dysfunction.
These renal tubular syndromes support a direct toxic effect of the virus on the tubular epithelium. The prevalence and consequences of tubular dysfunction in COVID-19 is worthy of further study.
References
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