Proteinuria After Kidney Transplantation, Relationship to Allograft Histology and Survival

Amer, Hatem; Fidler, Mary E.; Myślak, Marek; Morales, Pablo; Kremers, Walter K.; Larson, Timothy S.; Stegall, Mark D.; Cosio, Fernando G.

doi:10.1111/j.1600-6143.2007.02006.x

Cited by 179 publications

(191 citation statements)

References 32 publications

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“…In a recent study from our center, 45% of transplant recipients in general were found to have proteinuria (4150 mg/day), including 7% with proteinuria 41.5 g/day. 13 Therefore, C1q deposition may not be responsible for proteinuria in our patients. The milder clinical and pathological features associated with C1q deposition in the allograft compared with the native kidney are possibly due to the disease detection at early stages by protocol biopsies, the therapeutic effects of the maintenance immunosuppression regimens administered to prevent graft rejection, and/or the hemodynamic effects of calcineurin inhibitors.…”

Section: Discussionmentioning

confidence: 66%

“…This recommendation is based on recent data indicating that proteinuria after kidney transplantation, even at low levels (o500 mg/day), is associated with reduced graft survival, independent of glomerular pathology, graft function, and acute rejection. 13,15 In the recent study by Vizjak et al, 6 of 72 cases of C1q nephropathy in the native kidney, 37.5% of patients had underlying infections, most commonly upper respiratory tract infection. Furthermore, the single previously reported patient with de novo 'C1q nephropathy' in the renal allograft had concurrent BK polyoma interstitial nephritis.…”

Section: Clinical Featuresmentioning

confidence: 99%

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C1q deposition in the renal allograft: a report of 24 cases

et al. 2010

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C1q nephropathy is an uncommon glomerular disease characterized by dominant or codominant mesangial staining for C1q in the absence of systemic lupus erythematosus. There are no series in the literature addressing the significance of C1q deposition in the renal allograft. We retrospectively analyzed 24 patients, most of whom were white (83%) and male (63%), with a mean age at transplant of 31 years. None of the patients were diagnosed with C1q nephropathy in the native kidney or had any features of systemic lupus erythematosus. The mean time from transplant to detection of mesangial C1q deposits was 37 months (412 months in 71% of cases). Half of the patients had a preceding infection. The indication for biopsy was surveillance (63%) or graft dysfunction (37%). At biopsy, 52% had proteinuria (41g/day in only 17%). The mean creatinine was 1.8 mg per 100 ml. Only 9% developed hematuria and none had hypoalbuminemia. The glomerular pattern on light microscopy was mesangial hypercellularity (46%), focal segmental glomerulosclerosis (21%), or no lesions (33%). All cases showed intense (Z2 þ ) dominant (67%) or codominant (33%) mesangial staining for C1q on immunofluorescence. Mesangial electron-dense deposits were seen in 82% of cases. On follow-up (mean 1 year) of the 10 patients without rejection, most had stable creatinine with no or stable proteinuria, and none lost their graft. We conclude that C1q-dominant mesangial deposition in the renal allograft is a morphological pattern with no apparent clinical significance in the majority of patients. It is usually detected after the first year. The rate of preceding infection and the prevalence of proteinuria seem to be similar to the renal transplant recipients in general. Most cases show mesangial hypercellularity or no glomerular changes on light microscopy. Modern Pathology (2010) 23, 1080-1088; doi:10.1038/modpathol.2010.92; published online 14 May 2010 Keywords: C1q nephropathy; transplant; de novo glomerular disease; FSGS; proteinuria; mesangial hypercellularityIn 1982, Jones and Magil 1 reported five patients with proteinuria and nonsystemic mesangiopathic glomerulonephritis, one of whom had C1q codominant mesangial deposits. In 1985, Jennette and Hipp 2 introduced the term 'C1q nephropathy' and defined it as dominant or codominant mesangial staining for C1q in patients lacking clinical or serological evidence of systemic lupus erythematosus. In their report, which included 15 patients who presented in their second or third decade of life with nephrotic-range proteinuria, 100% of patients had proteinuria (range 1-24 g/day), 40% hematuria, 0% hypocomplementemia, and 0% positive antinuclear antibodies. The light microscopic findings varied from normal-appearing glomeruli to mesangial hypercellularity to endocapillary hypercellularity. On immunofluorescence (IF), all cases showed intense segmental or global mesangial staining for C1q, which was accompanied by equal or weaker staining for C3 and immunoglobulins. On electron microscopy, all cases showed mesangial ele...

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Section: Discussionmentioning

confidence: 66%

Section: Clinical Featuresmentioning

confidence: 99%

C1q deposition in the renal allograft: a report of 24 cases

et al. 2010

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“…In studies involving adult populations which used a very liberal threshold of 2-3 g/day, prevalence was only 10-15 % [5,7]. In contrast, studies that used a threshold similar to that used for non-transplanted patients (0.15-0.25 g/day) revealed proteinuria in 31-45 % of patients [4,11].…”

Section: Prevalence Of Post-transplant Proteinuria and Methods For Itmentioning

confidence: 97%

“…The prevalence of proteinuria reported in different studies on adult and pediatric populations varies considerable, from 11 to 82 % [4][5][6][7][8][9][10][11][12][13]. The main reason for this wide variation in prevalence of proteinuria is the different threshold used in these studies to define proteinuria.…”

Section: Prevalence Of Post-transplant Proteinuria and Methods For Itmentioning

confidence: 99%

Management of proteinuria in the transplanted patient

Seeman

2014

Pediatr Nephrol

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Proteinuria is a relatively frequent complication in children after renal transplantation (40-80 %). It is usually mild and non-nephrotic in nature and predominantly tubular in origin. The major causes of post-transplant proteinuria are recurrence of primary glomerulonephritis [mostly focal segmental glomerulosclerosis (FSGS)], rejection (acute and chronic), mTOR inhibitors or hypertension. Proteinuria is a risk factor for graft loss and patient death in adults, and even a mild proteinuria (0.1-0.2 g/day) is associated with impaired graft and patient survival. In children, proteinuria seems to be associated with graft but not patient survival. Proteinuria (protein/creatinine ratio) should be assessed regularly in all children. In children with prior chronic kidney disease due to idiopathic FSGS, proteinuria should be assessed daily during the first month after transplantation to enable early diagnosis of recurrence. The cause of proteinuria should be identified, and graft biopsy should be considered in children with unexplained proteinuria, especially with new onset proteinuria or deterioration of previously mild proteinuria. Treatment must be primarily targeted at the cause of proteinuria, and in normotensive children symptomatic antiproteinuric therapy with angiotensinconverting enzyme inhibitors/angiotensin II receptor antagonists should also be initiated. Other antihypertensive drugs should be used to achieve target blood pressure of<75th percentile. Target proteinuria should be <20 mg/mmol creatinine.

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“…Da mesma forma, a presença de proteinúria é um fator de risco associado à sobrevida do paciente e do enxerto em receptores de transplante renal. 35 A média da concentração de proteína em amostra isolada de urina foi de 0,52 g/dL no primeiro ano de transplante, com aumento gradual (58%) até 0,82 g/dL no quinto ano de transplante, sendo que nenhum paciente apresentou valores de proteinúria que ultrapassassem 1 g/L. Não podemos determinar se esse grau e incremento na proteinúria é consequência direta do uso de SRL, do desenvolvimento da disfunção crônica do enxerto, recorrência ou glomerulopatia "de novo" ou, o que é mais provável, uma combinação desses fatores.…”

Section: Discussionunclassified