The most commonly observed complication of KTx is allograft dysfunction that rarely may induce graft loss.
Kidney
allograft dysfunction
Abbreviations:
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.
The most commonly observed complication of KTx is allograft
dysfunction that rarely may induce graft loss. The timely
recognition & estimation of allograft dysfunction is crucial as it is commonly
reversible. However,
sustained dysfunction with the lack of a proper intervention may be complicated
by irreversible loss
of graft function and, ultimately, allograft failure. The etiology of kidney
allograft dysfunction may vary by time (can be classified into:
o
Immediate,
o
Early, &
o
Late period, post- Tx.
Currently, there’s no universal definition for an
allograft dysfunction after KTx. However,
we can define acute
kidney allograft dysfunction as one or more of the following:
o
Rise in SCr of
≥25 % from its baseline within 1-3-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 ≥25 % 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
potentially reversible causes 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.
Post Tx proteinuria
> 1 g/d
is a clear indicator of allograft dysfunction.
In the earlier post-Tx period, proteinuria could
be a Sn of recurrence of or de
novo FSGS that should promptly
evaluated. We usually perform a kidney graft biopsy in all
KTR presenting
with proteinuria > 1
g/d, regardless of the level of SCr, if it
is not currently contraindicated. The DD of kidney allograft dysfunction is currently
altered with the timing of presentation after Tx.
Specific causes of kidney allograft malfunction (e.g., surgical sequelae) are
more commonly observed in the immediate-to-early post-Tx
period, whilst other etiologies (e.g., viral infection) are more commonly
presenting later post-transplant. However, there is currently overlapping
etiologies among the timings of presentations, and certain factors of acute graft
dysfunction (e.g., Ac Rj) could be
seen at any time post-Tx.
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.
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