Adverse Effects Of Renal Post-Transplant Management

RENAL TRANSPLANT

Kidney transplant is a organ transplant to patient with an stage renal disease. And that end of 2003 renal transplants reached 1.7 million. Renal transplant is treatment of choice for chronic renal insufficiency. It promotes the patient’s quality and survival of life. Real transfer introduce the expenditure of dialysis on the health budget

POST TRANSPANT MANAGEMENT

Here is where you start discussing immunosuppresor and all the labs that need to be regularly checked and periodicity of the patient physician contact

Complications

AKA > Adverse effect of post-transplant management

Infections due to immunosuppression

Immunosuppression is a state in which established immunity and the response to new antigens are impaired (Bagshawe, 1972). The term covers changes in cell-mediated as well as in antibody-mediated immunity. The immunosuppressed state can have many causes ranging from spontaneous illness, particularly diseases of the lymph reticular system, to the deliberate use of immunosuppression, for example to counter graft rejection. It is not easy to separate the complications of immunosuppression from those of bone marrow suppression, for most immunosuppressive drugs also damage marrow cells; indeed of the immunosuppressive drugs only the steroid hormones seem not to be myelotoxic (Kay & Jameson, 1970).

In renal transplant, the clinical use of immunosuppression means that dermatologists can expect to be shown patients suffering from common infective conditions in an unusual form, or even from previously very rare infections. Most immunosuppressive agents lack selectivity, and interfere, to a variable degree, with both cellular and humoral immunity; but if a generalization is possible, it is that most of the case reports have been of viral, fungal and Gram-negative infections, suggesting that the main effect has been on cell-mediated immunity. However, it is with instances of skin disease that we are concerned here and these must be seen in perspective against the background of other infections.

In one study on infection after renal transplantation (Bach et al., 1973) involving fifty-one recipients of grafts, fifteen developed infections as complications, and of these, only two had skin infections, both also having infections of the lung with nocardia and aspergillus. Skin infection (22%) was less common than lung (42%) or urinary tract (35%) infection in another series of 216 patients with renal transplants (Eikhoff ef al., 1972). Turcotte (1972) looked for serious infections in ninety-three patients at risk for a total of 1000 months after transplant; among the serious infections were herpes simplex (6), cellulitis (4), and herpes zoster (3). Sometimes the features of the infection make diagnosis difficult. For example, of three patients described with skin infections during immunosuppressive therapy (Park, Goltz & Carey, 1967), one had persistent varicella, one an extensive, non-healing herpes simplex, and one a disseminated histoplasmosis with a widespread erysipelas-like rash.

Bacterial infections

Two renal transplant patients developed multiple subcutaneous abscesses due to M. cheloni (abscessus) (Graybill et al., 1974).

Skin ulcers may be infected with atypical mycobacteria and 'non-pathogenic' fungi as a complication of immunosuppressive therapy (Lomvardis & Madge, 1972).

TEN in adults: for example with deficient cell mediated immunity (Reid, Weston & Humbert, 1974); in a patient receiving prednisolone and azathioprine (Levine & Norden, 1972); in a patient with leukaemia (Hawley & Aronson, 1973; Norden & Mendelow, 1974); during renal failure (Hunter & Davison, 1973); in lymphoma patients (Caldwell, Montgomery & Peachey, 1967); and in heroin abuse (Lewis, 1974). Prednisolone and azathioprine have been shown to potentiate the appearance of TEN in baby mice challenged with phage group II Staph aureus; though no effect could be demonstrated on the action of the epidermolytic toxin alone (Wiley et al., 1974) and it seems clear that it is host resistance to the organisms which is impaired by the immvmosuppressive drugs. TEN also occurs in the apparent absence of staphylococci in patients with graft-versus-host reactions (Ammann & Tooley, 1972)

Escherichia coli septicaemia may cause toxic epidermal necrolysis (Plant & Mirani, 1972) or sub-epidermal bullae (Fisher, Berger & Keusch, 1974)- It is noticeable how often renal failure figures in these reports, including the patient who developed Norwegian scabies while on immunosuppression (Paterson, Allen & Beveridge, 1973).

An additional suppressive mechanism may be the inhibition of lymphocyte function caused by methyl guanidine which is present in high concentration in the plasma of uraemic patients (Harris et al., 1962).

Nothing seems to be known of the skin flora of patients suffering graft rejection, or who are acutely ill and receiving high doses of immunosuppressive agents, though those who are well maintained have a skin flora very like that of normal persons (Noble, Rebel & Smith, 1974).

It may be that many of the organisms are from the patient’s own, endogenous, gut flora, yet it is these organisms that proliferate on the skin of severely ill patients (Gallus, Stratford & Dixson, 1969).

We may speculate that in some diseases associated with immunosuppression, the skin may be the portal of entry for pathogens; indeed. Spiers (1974) reporting death from septicaemia in three of four patients with leukaemia or lymphoma who had initially been merely colonized with Pseudomonas aeruginosa suggested that 'Isolation of pseudomonads from any cutaneous lesion, however minor, is an Indication for systemic therapy

Viral infections

Herpes simplex after renal transplant may be unusually extensive, haemorrhagic and persistent; in four affected patients (Montgomerie et al., 1969) the herpetic infection caused the death of one individual and was an important factor in the death of the other three. Severe herpes simplex has also been seen in patients with lymphoma (Lynfield, Farhangi & Runnels, 1969).

The well-known susceptibility of patients with atopic eczema to herpes simplex and vaccinial infections, and now apparently to dermatophyte infections (Jones, Reinhardt & Rinaldi, 1974) may also relate to abnormal cell-mediated immunity. Experimentally, herpes simplex can be recalled in mice by the administration of prednisone, though lesions do not reappear for 12-30 days (Underwood & Weed, 1974).

Other viruses also flourish. It has been suggested that the appearance of luxuriant warts should suggest the possibility of immune deficiency (Perry & Harman, 1974).

Brodersen, Genner & Brodthagen (1974) in a study of tuberculin sensitivity found that children with warts had a mean zone of induration of 10 mm compared with about 15 mm in controls. They point out that it is not possible to decide whether the reduced sensitivity results from the wart infection or whether the warts are a marker for a defective cellular immunity.

Molluscum contagiosum has been recorded in two patients treated with methotrexate and prednisone (Rosenburg& Yusk, 1970)5 each patient having about 600 lesions.

Varicella was reported in a child treated with azathioprine (Fine et al., 1969) and Armstrong and his colleagues (1970) were able to relate the death of cancer patients who developed varicella to a failure to produce high levels of interferon. Three patients were leukopenic, and two died from the infection; while four other patients who were not leukopenic produced, high levels of interferon and all recovered.

Cytomegalovirus seems also to be an important cause of infection (Kanich & Craighead, 1966; Rifkind, Goodman & Hill, 1967a), particularly of the eyes of immunologically compromised patients (Porter et al., 1972).

Renal transplant patients also show an increased excretion of the Epstein-Barr virus (Strauch et al., 1974). A giant orf lesion has been described in a patient receiving immunosuppressive agents (Savage & Black, 1972). Finally, there is a possibility that the high incidence of tumours of the lympho-reticular system that is found in immunosuppressed patients may be due to the uncontrolled proliferation of oncogenic viruses (Allison, 1970).

Fungal infections

Fungal infections are expected to be more prevalent in renal transplant recipients, because these patients take immunosuppressive agents to enhance graft survival. Previous studies investigated a wide spectrum of cutaneous disorders in these patients. In one case-control study with 102 renal transplant recipients revealed a higher prevalence of fungal infection in patients (63.7%) than in immunocompetent controls (30.7%). pityriasis versicolor was the most common fungal infection (36.3%) in the group of renal transplant recipients in this study. Next in order of frequency were oral candidiasis (25.5%), onychomycosis (12.7%), and fungal toe-web infection (11.8%). Other authors have indicated that there is a high rate of colonization with Pityrosporum organisms in renal transplant recipients

Unusual fungi have been particularly troublesome in some patients

A Phoma species caused a subcutaneous abscess in an immunosuppressed patient (Young, Kwon-chung & Freeman, 1973). Primary cutaneous aspergillosis has been recorded in the absence of chemotherapy (Cahill, El Mofty & Kawaguchi, 1967) but could be increased in compromised patients in the same way that limg infections become especially common (Gowing & Hamlin, i960; Gurwith et al., 1971; Stinson et al., 1971; Burton et al., 1972; Burton & Greenough, 1973).

Roberts (1969) reported that systemic corticosteroid therapy was associated with an increased susceptibility to pityriasis versicolor. It may be significant that three of six seriously ill patients, in a total of twenty-five new patients, were receiving azathioprine, two for renal disease. The association of candidiasis with systemic steroids is too well known to need much comment here. Skin lesions may appear in neutropenic patients who have Candida septicaemia but do so only in those with an easily demonstrable blood stream infection (Bodey & Luna, 1974). Diffuse severe thrombocytopenic purpura has been reported in two patients with histoplasmosis; transfer from the first patient to the second appeared to be due to the renal transplant (Hood et al., 1965).