Late onset granulomatous interstitial nephritis after booster dose of COVID-19 vaccination: Case report and review of literature.

Billions of doses of COVID-19 vaccine have been administered to combat the coronavirus pandemic. Though the vaccine is generally well tolerated, several cases of new onset or relapsing glomerulonephritis have been reported. In comparison, post-vaccination tubulointerstitial nephritis (TIN) has rarely been reported, mostly after the first or the second dose of the vaccine. Acute interstitial nephritis after booster dose of COVID-19 vaccination has not yet been reported. We report a case of acute granulomatous TIN shortly after the booster dose of Moderna vaccine. Our patient had no clinical evidence of renal injury after the first two doses of vaccine. Renal dysfunction was incidentally observed ~ 1 month after the booster dose of vaccine. The patient responded to steroids with rapid improvement in kidney function. While it is difficult to ascertain the causal relationship between the vaccination and development of TIN, it is important to be vigilant about such delayed side effects of the vaccine.

Post-renal transplantation hypophosphatemia: a review and novel insights.

PURPOSE OF REVIEW: This review intends to elucidate the pathophysiologic mechanism of renal phosphorus loss in the post-renal transplantation population. This review will provide new insight in to the pathophysiologic mechanism(s) responsible for the development of this phenomenon and will also explore the pathogenetic role of persistent phosphorus wasting in the development of post-renal transplantation osteodystrophy. RECENT FINDINGS: Recently, the phosphaturic hormone, fibroblast growth factor-23, has been ascertain to be increased in the sera of patients with chronic kidney and end-stage renal disease. There is new evidence that a non-PTH humoral factor is persistently present in post-renal transplantation patients that is likely responsible for the observed persistent renal phosphorus loss. We offer that fibroblast growth factor-23 (and/or other phosphatonins) is the culprit factor responsible for the phenomenon of persistent hypophosphatemia in post-renal transplantation patients. Moreover, we believe that the phenomenon of persistent renal phosphorus wasting is an important but overlooked cause of osteodystrophy and increased fracture risk in this patient population. SUMMARY: The pathophysiology of post-renal transplantation phosphorus wasting is complex and to date is still not fully recognized. Further studies of the regulatory mechanism of fibroblast growth factor-23 and its metabolism may offer additional insights into phosphorus homeostasis and its clinical application in the post-renal transplantation population.