By D. Josh. Stephens College. 2018.
Cyclosporine therapy has made no difference in the branous glomerulonephritis reported in 2% to 5% of transplantations incidence of the two entities buy cheap cytotec 100mcg on-line, and hepatitis C virus infection may be is often asymptomatic and usually associated with chronic rejection associated with membranous disease after transplantation generic cytotec 100mcg line. FIGURE 17-30 FIGURE 17-31 (see Color Plate) H istologic slide of a biopsy showing extensive spike form ation H istologic slide showing deposition of anti–glom erular basem ent along the glomerular basement membrane cheap cytotec 200 mcg otc. This woman had recurrent m em brane (GBM ) antibody along the GBM , which is seen in over membranous disease 8 months after transplantation. In most of these Both recurrent and de novo m em branous glom erulonephritis are cases no histologic abnormalities are seen within the glomerulus, how- indistinguishable from idiopathic m em branous nephropathy. The ever, and patients remain asymptomatic with normal renal function. Delaying transplantation for at least 6 m onths after antibodies have becom e undetectable reduces the recurrence rate to only 5% to 15%. Treatm ent of the prim ary disease with antibody deposition in anti-GBM disease is diffuse and global and, in plasm a exchange, cyclophospham ide, and steroids leads to rapid practice, is rarely confused with the nonspecific antibody deposition loss of circulating antibodies. Patients who need transplantation seen in other conditions. In chronic transplantation glom erulopathy while circulating antibodies are still detectable should be treated the antibody deposition is focal and segmental, and focal necrosis and with plasm a exchange before and after transplantation to m inim ize cellular crescents are extremely rare. The finding of linear antibody circulating antibody levels and with cyclophospham ide therapy for deposits on a transplantation biopsy should lead to testing for 2 m onths. A sim ilar approach should be used in patients with clini- circulating anti-GBM antibodies. Patients who have linear im m unoglobulin deposi- along with linear IgG staining, m ay be the first indication that a tion in the absence of focal necrosis, crescents, or renal dysfunction patient with an unidentified cause for end-stage renal disease has do not require treatm ent. After transplantation, approxim ately 15% of Chromosome Collagen Diseases caused by mutations patients develop linear deposition of im m unoglobulin G (IgG) along the glom erular basem ent m em brane (GBM ), and circulating 13 1 and 2 chains of type IV anti-GBM antibodies specific for the 3 or 5 chains of type IV 2 3 and 4 chains of type IV Autosomal recessive or dominant collagen [42–44]. Those patients who do develop proteinuria or hem aturia usually lose their grafts. In som e cases, treatm ent with cyclophospham ide did not prevent graft loss. The incidence of H US recurrence is difficult to assess. At one extrem e, five of 11 children suffered graft loss because of recurrent disease. H owever, m ost series have reported substantially lower recurrence rates: no recurrences in 16 adults and children, one of 34 grafts in 28 children, and two probable recurrences of 24 grafts in 20 children [4,45,46]. Graft loss occurs in 10% to 50% of patients with recurrence. HUS has been diagnosed 1 day to 15 months after transplantation (usually in less than 2 months), and the incidence of recurrence is increased in patients receiving grafts less than 3 months after their initial disease. Treatment of recurrent disease is plasma exchange for plasma or cryosupernatant, or plasma infusions, and dose reduction of cyclo- sporine. Recurrence may be prevented by aspirin and dipyridamole. FIGURE 17-36 DIFFERENTIAL DIAGNOSIS OF RECURRENT Blood film abnorm alities, m icroangiopathic hem olytic anem ia, HEM OLYTIC UREM IC SYNDROM E throm bocytopenia, and acute renal failure occur in accelerated hypertension and acute vascular rejection. A renal biopsy usually distinguishes acute vascular rejection, and malignant hypertension Thrombotic microangiopathy associated with cyclosporine should be obvious clinically. The m icroangiopathy of cyclosporine Acute vascular rejection can be difficult to differentiate from hemolytic uremic syndrome; however, glom erular pathology usually is less m arked and vascular Accelerated phase hypertension changes m ore obvious with cyclosporine toxicity. D e novo Tacrolimus- (FK-506) associated thrombotic microangiopathy hem olytic urem ic syndrom e also has been reported in patients treated with tacrolim us (FK-506). Very few patients with system ic sclerosis have received inhibitors after transplantation is unknown. Two of four patients transplantation, and the incidence of acute renal failure caused by with im m unotactoid glom erulopathy developed recurrent disease systemic sclerosis has declined with the widespread use of angiotensin- heralded by m assive proteinuria. About 20% of patients with a rarely leads to graft-related problem s; however, patients die from m alignant course of scleroderm a receiving a transplantation develop system ic com plications of ceram ide deposition. For patients with prim ary hyperoxaluria, Disease Treatment of recurrence m easures to prevent further deposition of oxalate have proved successful in controlling Focal segmental glomerulosclerosis Plasma exchange, immunoadsorption, steroids, recurrent renal oxalosis. In diabetes angiotensin-converting enzyme inhibitors, m ellitus, the pathophysiology of recurrent nonsteroidal anti-inflammatory drugs nephropathy undoubtedly reflects the sam e Immunoglobulin A nephropathy W ith crescents: plasma exchange, cytotoxics insults as those causing the initial renal failure, Henoch-Schonlein purpura? Steroids and good evidence exists that glycemic control Mesangiocapillary glomerulonephritis type I Aspirin, dipyridamole can slow the development of end-organ Mesangiocapillary glomerulonephritis type II? Plasm a exchange and im m uno- Membranous nephropathy? Cytotoxics and steroids adsorption are prom ising therapies for Anti–glomerular basement membrane disease Plasma exchange, cyclophosphamide patients with nephrosis who have recurrent Hemolytic uremic syndrome Plasma exchange, plasma infusion focal segmental glomerulosclerosis; however, Antineutrophil cytoplasm antibody–associated vasculitis Cyclophosphamide and steroids these therapies do not provide sustained Diabetes Glycemic control remission [6,7]. In all these cases, establishing Oxalosis Aggressive perioperative dialysis, hydration, low oxalate a diagnosis of recurrent disease is critical in diet, low ascorbic acid diet, phosphate supplements, identifying a possible treatm ent m odality. Even excluding these conditions, the overall rate of recurrence of glomerulonephritis is substantially increased in living related donors, Focal segmental glomerulosclerosis with risk factors for early recurrence and patients should be m ade aware of this risk. For fam ilial Henoch-Schonlein purpura diseases, the risk of recurrence is even higher (eg, som e fam ilies with im m unoglobulin A disease and hem olytic urem ic syndrom e). Mesangiocapillary glomerulonephritis type I Finally, recurrent glom erulonephritis has been reported in up to Mesangiocapillary glomerulonephritis type II with risk factors (familial immunoglobulin A nephropathy and hemolytic uremic syndrome) 30% of renal isografts, with disease onset between 2 weeks and 16 years after grafting. Tejani A, Stablein DH: Recurrence of focal segmental glomerulonephritis 7.
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