Proteinuria Management in Kidney Transplantation

Proteinuria following kidney transplantation remains a pivotal marker of graft injury and a predictor of long-term graft survival. Its onset may reflect a spectrum of underlying processes, ranging from immunological injury—such as antibody-mediated rejection, transplant glomerulopathy and recurrent or de novo glomerulonephritis—to non-immunological factors including donor characteristics, ischaemia–reperfusion injury and podocyte dysfunction. Early identification relies on quantitative assessment of urinary protein, traditionally via 24-hour collections but increasingly through spot urine protein-to-creatinine ratios and estimated protein excretion rates. Histopathological evaluation of graft biopsies, often guided by Banff criteria, elucidates the dominant lesions and informs tailored adjustments of immunosuppression. Management strategies focus on minimising immunological triggers through optimisation of maintenance regimens, judicious use of steroid pulses or plasmapheresis in acute injury, and blockade of the renin–angiotensin–aldosterone system to reduce intraglomerular pressure and protein leak. Emerging insights into podocyte biology, genetic predispositions and donor proteinuria suggest potential for personalised risk stratification. In aggregate, an integrated approach that combines precise monitoring, immunomodulation and adjunctive therapies is central to mitigating proteinuria and preserving graft function on a global scale.

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Proteinuria Management in Kidney Transplantation publication trend

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Technical terms

Proteinuria: Excessive excretion of protein in urine, indicating glomerular or tubular injury.

Nephrotic-range proteinuria: Urinary protein loss exceeding 3.5 g/day, often associated with hypoalbuminaemia and oedema.

Estimated protein excretion rate (ePER): A calculation of daily protein loss derived from spot urine protein-to-creatinine ratio.

Glomerular filtration rate (GFR): A measurement of kidney function reflecting the volume of filtrate produced per minute.

Renin–angiotensin–aldosterone system (RAAS) blockade: Use of ACE inhibitors or ARBs to reduce intraglomerular pressure and proteinuria.

Banff criteria: An internationally recognised histopathological classification system for renal allograft pathology.

Transplant glomerulopathy: Chronic injury to the glomerular capillary wall characterised by reduplication of the basement membrane.

References

1. Consequences of Nephrotic Proteinuria and Nephrotic Syndrome after Kidney Transplant. Biomedicines (2024).
2. Relationship between early proteinuria and long term outcome of kidney transplanted patients from different decades of donor age. BMC Nephrology (2019).
3. Association Between a TLR2 Gene Polymorphism (rs3804099) and Proteinuria in Kidney Transplantation Recipients. Frontiers in Genetics (2022).
4. The Prevalence of Immunologic Injury in Renal Allograft Recipients with De Novo Proteinuria. PLOS ONE (2012).
5. First and second morning spot urine protein measurements for the assessment of proteinuria: a diagnostic accuracy study in kidney transplant recipients. BMC Nephrology (2021).
6. Donor Proteinuria and Allograft Function in Kidney Transplantation: Short- and Long-Term Results From a Retrospective Cohort Study. Transplant International (2023).