The most commonly observed complication of KTx is allograft dysfunction that rarely may induce graft loss.
o Ac Rj: Acute rejection.
o CNI: calcineurin inhibitor.
o DD: differential diagnosis
o DGF: Delayed graft function.
o Dgx: Diagnosis.
o DX: Dialysis.
o FSGS: focal segmental glomerulosclerosis.
o KTR: kidney transplant recipients
o KTx: kidney transplantation
o Post-Tx: post-transplant.
o Pn: Pyelonephritis.
o RAS: renal artery stenosis.
o SCr: serum creatinine.
o Ttt: Treatment.
o UO: urine output.
o USS: ultrasound study.
o FSGS: focal segmental glomerulosclerosis.
o GN: Glomerulonephritis.
o MN: membranous nephropathy.
o MPGN: membranoproliferative GN.
o Dc Np: diabetic nephropathy.
o IgA Np: immunoglobulin A nephropathy.
o NRP: nephrotic-range proteinuria.
o CAN: Chronic allograft nephropathy.
o IFTA: interstitial fibrosis/tubular atrophy.
o Rise in SCr of ≥ % from its baseline within -mo,
o Lack of SCr decline after Tx, and/or
o Proteinuria >1 g/d.
- DGF can be defined as DX requirement within the 1st week after Tx.
- Chronic kidney allograft dysfunction = condition with irreversible damage to the kidney allograft seen over weeks to months duration.
A suggested approach for assessing and Dgx of kidney allograft dysfunction is relying primarily on the timing of presentation. A Dgx can be settled in most ptns via a thorough history taking as well as physical examination, lab & image testing, and/or lastly resorting to an allograft biopsy.
o Ptns experiencing allograft dysfunction within 1st week Post-Tx most commonly present with low UO or failure of the SCr decline after Tx. Some ptns (i.e., those with DGF in particular) may require DX in the 1st week after Tx. Proper assessment & Dgx of the cause of allograft dysfunction is crucial as certain factors of acute graft malfunction (e.g., thrombotic events) in the immediate postoperative period can be complicated with a higher risk of allograft loss. Vascular causes of graft dysfunction within the 1st week are representing Tx emergency, and it is mandatory to recognize that the renal allograft is adequately perfused.
o In KTR presenting after the 1st week Post-Tx with a new rise in SCr of ≥ % from baseline or a SCr that is extremely higher than expected (e.g., in recent Tx ptns with SCr is continuing to decline after Tx), we proceed an initial work-up for assessing the of allograft dysfunction (e.g., Pn, fluid deprivation, nephrotoxic agents, CNI nephrotoxic members). In ptns with NO recognized potential cause or those with SCr cannot return back to baseline after ttt and resolving these potential factors of graft dysfunction, proceed to a kidney allograft USS + Doppler to assess for the presence of a perinephric fluid collection (e.g., urine leak (urinoma), perinephric hematoma), obstructive uropathy, or Tx RAS.
-If USS showed any abnormality that could declare the rise in SCr, then, accordingly we manage with the proper therapy (e.g., drainage + assessment of fluid collection, angioplasty of Tx RAS) and frequent measuring of the SCr. If the SCr remains persistently high in spite of initial successful interference of the lesion diagnosed via USS, we proceed a kidney allograft biopsy. If the USS testing is negative for obstructive lesions or other causes, we proceed to a kidney allograft biopsy.
Recurrent primary disease: Ptns with primary GN kidney disease, recurrent disease must be considered as a possible explanation of allograft dysfunction. The rate of recurrence is varying according to the specific GN disease. GN lesions is commonly recur post-Tx and include primary FSGS, primary MN, MPGN, complement-mediated HUS, as well as C3 glomerulopathy. Latly recurred GN (i.e., > one y. post-Tx) could be frequently seen and include FSGS, MPGN, IgA Np, as well as Dc Np. Biopsy of the kidney allograft is mandated for Dgx.
De novo glomerular disease: Although GN diseases that reported in the Tx kidney are frequently recur, the primary disease involving the native kidney may differ from a de novo GN that are unrelated to the original disease affecting the native kidneys. The clinical presentation & histological features of the de novo GN are generally simulating those seen in ptns with primary or secondary GN in the native kidneys. These include a rise in SCr, proteinuria, hematuria, in addition to an active urine sediment.
Chronic allograft nephropathy: = CAN; also called IFTA, is a poorly identified lesion that can be defined as kidney allograft dysfunction (seen at least 3 mo. post-Tx) with lack of:
o Active acute rejection,
o Drug toxicity (mainly CNI), or
o Any other associated disease.
The clinical Dgx is usually suggested by gradual decline of allograft function, as clinically manifested by a slowly elevated SCr level, rising proteinuria (sometimes NRP), and deteriorated HT.