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Q.777.What is the Graft-versus-host disease (GVHD)? How it could affect the kidneys?


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Renal transplantation- Allograft


Q.777. What is the Graft-versus-host disease (GVHD)? How it could affect the kidneys?

A. GVHD occurs when immune cells transplanted from non-identical donor (graft) recognize the Tx. recipient (host) as foreign, thereby initiating an immune reaction that causes disease in Tx recipient. Ac. GVHD typically involves: {the skin, G.I.T. & liver, hematopoietic system & kidneys.}.

Dgx of Ac. GVHD cn be made readily on clinical grounds in ptn. who presents é [Classic maculo-papular rash, abdominal cramps é drr. &rising s. bilirubin é 1st100 d. following hematopoietic cell Tx. (HCT), us. within 2-3 w. foll. HCT]. Many cases, however, Dgx is less straightforward & competing causes for isolated abnormal must be considered and excluded. Hist. confirmation can help to get clinical impression of possible Ac. GVHD. Severity of Ac GVHD is determined by assessment of degree of involvement of: skin, liver & GIT. This’s subsequently combined é results on performance scales to produce an overall grade. G. I GVHD is ch.ch. as mild disease., II as moderate, III: severe & IV life-threatening.

Renal dis.: With Ac. GVHD, induction of autoimmune dis. occ. in associated é auto-AB. production may require expression of specific class II haplotypes. In murine model of GVHD, onset of lupus-like nephritis in animals producing pathogenic IgG anti-nuclear A.B. was dependent upon the MHC haplotype expressed by recipients. There’re isolated case rep. of ptn é Ac. and/or ch. GVHD who develop N.S. due to membranous nephropathy. Murine models of GVHD support a direct pathogenetic association. Most ptns hv hd stabilization in R. function& significant. reductions in protein excretion after ttt. é steroids and/or Csp..

N.B.  Dermatologic Disorders Ass. With R. Tx.

50-100 % of R. Tx. recipients (RTRs) hv Tx-related cutaneous complaint. Dermatologic diso. ass. é R. Tx. are a function of im/m. medications prescribed, as well as the im/m. condition produced. Factors such as time after Tx., geographic location, climate, and skin type greatly modify the clinical disorders ass. é R..Tx.


1)   Cushingoid changes.

2)   Gingival hyperplasia.

3)   Disorders of the pilosebaceous unit, include: {acne, folliculitis, hypertrichosis, keratosis pilaris, sebaceous gland hyperplasia, epidermal cysts}. A full-blown Cushingoid appearance in 55-90% é high dose steroids used early after Tx.. Cutaneous findings include: moon facies, developed of cervical fat pad (buffalo hump), striae distensae, cutaneous atrophy & telangiectasias. Changes may resolve or improve when steroid dose is reduced, although these cutaneous changes may continue, as steroids are used long term. Gingival hyperplasia that occurs in one third of ptns receiving Csp, occurs early & improve over time. Other cutaneous changes involve poorly understood alterations in the pilosebaceous unit & result fr. either Csp. or steroid use. Acne develop in 15% of ptns and primarily affects chest & back. Most severe é 1st y., acne later improves é reduction of steroid dose. Sebaceous gland hyperplasia & epidermal cysts are found é increase frequency é use of both steroids & Csp. Hypertrichosis (60%) of ptns and ass. é develop of keratosis pilaris.


1)    Viral infc., incl.: HSV, VZV, EBV.

2)    Bacterial infection.: S. aureus, Bartonella henselae, mycobacteria, M. T.B. & atypical mycobacteria.

3)    Fungal infection: superficial mycoses (eg, dermatophytes, Pityrosporum species, candidiasis) and deep fungal infections (eg, Aspergillus, Cryptococcus, Nocardia, Rhizopus species).

4)    Parasitic infection, incl. scabies

5)   Actinic keratoses

6)    Malignancies: Squamous cell & basal cell carcinoma, keratoacanthoma, Kaposi sarcoma, melanoma.

7)    Miscellaneous: lymphoma, Merkel cell carcinoma (MCC) & dermatofibrosarcoma protuberans

8)    Miscellaneous diso.: transfusion-ass. graft-versus-host disease & porokeratosis


 Iatrogenically induced dcrease in cell-mediated immunity predisposes RTR to infection. Timing & relative risk of infection are determined by degree of im/m.. Ptns are at heightened risk for develop opportunistic infc. é 1st  6 m. due to use of higher doses of im/m. Skin exam. is crucial, as cutaneous lesion frequently: 🠞the first Sn of disseminated dis.. Mycobacterial: Later in the post-Tx period, ptn dev. infections fr. a variety of acid-fast bacilli (AFB), sp. typical or atypical mycobacteria. Although relatively unusual, they can cause significant morbidity. Multifocal dis. is not uncommon. M. fortuitum/chelonae cx are more common causes of AFB skin infection, alth. M. kansasii & M marinum, hv also bn reported. Histopathologic examination & tissue culture are necessary for correct Dgx. ttt.: {antimicrobials, surgical debridement, and/or dcrease im/m. dose}. Fungal: 🠞 most common cause of infc. in RTR (7-75) %. Variable prevalence results fr. heterogeneity in diagnostic criteria, environmental, geographic, economic & hygienic f. Pityriasis versicolor: the most common fungal infc. (18-48)% of RTR, which’s  higher rate thn in general population. Colonization of upper back é Pityrosporum yeasts occur 2-3 times more often in RTR. Pityrosporum org. may predispose to folliculitis. Dermatophytosis, alth. common after R. Tx., is no more common than general population. Viral: Sev. viral infc. us. occ é 1st  y. after Tx. & esp. herpes viruses. Skin lesions resulting fr. infc. é human papillomavirus (HPV) develop later. Surveys sugg.: HPV = 15-50% after 1st  y. & increase to 77-95% by 5 y. after Tx. Common & plane warts, wch predominate, occur most frequently in sun-exposed areas & us. multiple. HPV types 1, 2, 3 & 4 are found most commonly; however, many other HPV types ha ebeen rep. in ass. é warty lesions in RTR, incl. oncogenic types 16,18 , 5 & 8, which usually ass. é epidermodysplasia verruciformis. Eradication of HPV is difficult, as lesions respond poorly to therapy & recur frequently. Treating warts early & aggressively is best in RTR using routine modalities, e.g. cryotherapy, electrocoagulation & Co2 laser. Surgery & radiotherapy are not more effective and may result in scarring. Oral/topical retinoids may be an option. Interferon alfa, wch hs bn effective agnst warts in im/m. individuals, shd not be used in the RTR, as it may trigger allograft rejection. Imiquimod, cn heighten the host's immune system by upregulating interferon, ws thought to be similarly C.I. in Tx.. but more recent studies 🠞 both effective & safe when used in a limited fashion.  


More common after organ Tx., mostly cutaneous. Incid. of nonmelanoma skin cancer is 20-40 times greater in RTRs thn in general population. Incid. incr. as time elapsed. Cumulative risk of cutaneous malignancy is 10-30% at 5 y.s, 10-44% at 10 y.s, and 30-40% at 20 y.s. Prevalence of skin cancer varies acc. to geographic location, amount of UV light exposure &  predominant skin type. Most malignancies occ. on sun-exposed areas (head, neck & upper extremities). Multiple malignancies are a common. Nonmelanoma cancer: Squamous cell carcinoma (SCC): the most common skin malign-ancy, occur 50-250 times more frequently thn general population. In contrast, basal cell carcinoma (BCC) occ. 6-10 times more frequently in RTRs. As a result of the markedly incr. incid. of SCC, an inversion is sn in the ratio of BCC to SCC, fr. 4:1 in general population to 1:3-4 in RTRs. The image below illustrates SCC. Nonmelanoma malignan-A hyperkeratotic plaque on this RTRs ws proven to be SCC. Similar lesions frequently mistaken for warts.

cies occ. at a younger age and ch.ch. by more rapid & aggressive course, a higher recur-ence rate, and a greater metastatic potential. Actinic keratoses also occ. at a younger age and dev. faster in RTRs. Actinic keratoses frequently have more severe cytologic atypia & hv more rapid progression to SCC. Clinically, it may be difficult to distinguish actinic keratoses, SCCs, and warts. Factors predisposing to dev. of non-melanoma skin cancer includes: {exposure to UV light, skin phototypes I & II, im/m. & possibly, HPV infc.}. Most cancers occur in sun-exposed areas in lightly pigmented ptns. Im/m. drugs reduce cell-mediated immunity and, thereby, greatly augment the potential for malignant transform-ation. Whether Csp. is more or less oncogenic thn Aza remains controversial, because available data are conflicting. Aza & its metabolites are mutagenic and toxic to Langer-hans cells, but Csp is more im/m. One study found: siros may dcrease rates of skin cancer in RTRs. Compared to a CNI, Siros is ass. é significant lower yearly skin cancer rates in RTRs é history of nonmelanoma skin cancer.The role HPV may play remains obscure, because data are not conclusive; however, multiple HPV strains hv bn documented in many cutaneous malignancies, and malignant transformation of warty lesion has been obser-ved. Management of nonmelanoma skin cancers incl.:{Sun avoidance, use of broad-spectrum sunscreens, early detection of malignant & precancerous les., & aggressive therapy}. Complete surgical excision é margin control is necessary. Adjuvant radio-therapy/chemotherapy may hv a role in ass. é surgery in certain ptns. Some studies have shown imiquimod to be safe & effective for superficial BCCs & actinic keratoses when used on small surface areas acc. to directions; however, the safety & efficacy of this ag. in im/m. ptn. hv not bn established. Some authors advocate switching fr. Csp or tacrs to siros in hope of dcrease cancer risk. Be aware that minimizing  (UVB) exposure adds further risk for vit. D deficiency. Chemoprevention using systemic retinoids shd be reserved for high risk ptns for multiple malignancies. Partial & complete remissions hv bn rep. é retin-oid use, but long-term therapy is necessary, because the beneficial effect is lost 2-3 m. after stopping ttt. Adverse effects may preclude retinoid use. Potential adverse effects incl.: birth defects, hyperlipidemia & osteoporosis. In addition, CS & Csp. use frequently are ass. é hyperlipidemia & osteoporosis; concern exists that these effects may be amplified by addition of a retinoid. Reduction or discontinuation of im/m. should be consid-ered but may not be acceptable in some ptns because it may result in allograft Rj & loss. Kaposi sarcoma: 400-500 times higher in RTRs & accounts for 3-5% of Tx-related malignancies in RTRs. Incid. varies acc. to geographic region & depends on ethnic composition. Generally, Kaposi s. is higher in those é Jewish, Mediterranean, or Arabic ancestry and in blacks. The highest incid. is in 1st  y. after Tx. Kaposi sarcoma us. occurs 2-24 m. after Tx, in contrast to late dev. of most other Tx-related malignancies. As in other populations studied, dev. of Kaposi sarcoma in RTRs is ass. é human herpes v. 8 (HHV-8). Mucocutaneous lesions occur in 60% of Kaposi sarcoma ptn. & may be isolated in these areas; however, visceral dis. is not uncommon, ttt. options include {Cessation of im/m. medications, radiotherapy, chemotherapy, excision & cryotherapy}. Although complete regression hs bn described after discontinuation of im/m. therapy, adjuvant therapy usually needed. Kaposi sarcoma could be fatal due to “visceral involvement. Melanoma: 2-9 times more frequently in Tx. population than in general population. Interestingly, risk of melanoma in RTRs incl. transmission by the donor. Other malignancies: Alth. Kaposi sarcoma is the most commonly rep. sarcoma in RTRs, other cutaneous sarcomas have been rep.. Malignant fibrous histiocytomas, atypical fibroxanthomas & dermatofibrosarcoma protuberans hv bn rep.. Several cases of Merkel cell carcinoma (MCC) have been rep.. Most les. dev. on head & neck or the extremities. This’s an aggressive tumor é high propensity to recur or metastasize. Overall M.R. é MCC is 35%. Interestingly, reports exist of SCC & MCC occur simultaneously. Although lymphomas are 2nd most common malignancy in RTRs, cutaneous lymphomas are relatively rare. Whereas cutaneous T-cell lymphomas have been described, cutaneous B-cell lymphomas are more common in Tx. population.

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