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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2002  |  Volume : 13  |  Issue : 3  |  Page : 320-330
Tuberculosis and Chronic Renal Disease


Departments of Nephrology and Dialysis, Al-Hada Armed Forces Hospital, Taif, Saudi Arabia

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How to cite this article:
Hussein M, Mooij J. Tuberculosis and Chronic Renal Disease. Saudi J Kidney Dis Transpl 2002;13:320-30

How to cite this URL:
Hussein M, Mooij J. Tuberculosis and Chronic Renal Disease. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2019 Jul 18];13:320-30. Available from: http://www.sjkdt.org/text.asp?2002/13/3/320/33799

   Introduction Top


There is an increased incidence of tuber­culosis (TB) in patients with end-stage renal disease as compared with the general popu­lation. In absolute numbers, this observa­tion is especially important in areas where the disease is endemic. The presentation of TB in uremic patients is often quite unusual and insidious. Moreover, the diagnosis and management of TB in such patients provide the treating physician with many special challenges. Several aspects of tuberculosis in chronic renal failure (CRF) will be reviewed here.

Epidemiology

In 1997, It was estimated that about 7.96 million new cases of tuberculosis occurred worldwide; more than half were in Southeast Asia. [1] In North-America and Western­Europe, the incidence of TB was less than 10 per 100,000 general population, and the prevalence less than 20 per 100,000 while in the same report, the incidence and prevalence were 46 and 73 per 100,000 population, respectively, in Saudi Arabia. [1] Earlier in 1994, Al-Kassimi estimated the incidence of TB in Saudi Arabia as 30 per 100,000 population. [2]

The first report about increased prevalence of tuberculosis in dialysis patients appeared in 1974. [3] Later, many studies, of which several are summarized in [Table 1], have confirmed an increased risk of TB in patients with chronic renal failure and on dialysis in comparison to the general population, varying from 6.9 up to 52.5 fold. [4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30] The highest risk (100 fold) reported was from a center in London with a high immigrant population. [31]

Despite the well known association between diabetes mellitus and tuberculosis, especially pulmonary TB, [32] only two studies found a higher prevalence of tuberculosis in dialysis patients with diabetes mellitus, as compared with other renal diseases. [23],[31] Tuberculosis in dialysis patients has been seen in all age groups, although the mean age of the patients with TB was found slightly higher than that of the whole dialysis population. [12] However, a study from Taiwan, reporting on 122 dialysis patients with tuberculosis, found that such patients were younger than those of the general population. [9]

Besides studies on hemodialysis patients, there were two studies, which described exclusively peritoneal dialysis (PD) patients with TB; one in children with prevalence of 5.7% [26] and another in 790 patients on continuous ambulatory peritoneal dialysis (CAPD) with prevalence of 4.8% that was as high as in hemodialysis patients; TB peritonitis comprised 37% of the TB cases in them. [30]

There is no definite gender preponderance in the reported TB cases in CRF patients. Several studies mentioned high frequency of TB cases discovered in the first year of dialysis, [5],[7],[12],[15],[16],[18],[19],[23],[29] which has been attributed to the poor general health and compromised host immunity in these patients during that stage.

Pathogenesis

The host-response against intracellular pathogens, including Mycobacterium tuber­culosis, is determined by the T-cell helper type 1 response with the involvement of interleukin 12 that results in increased production of interferon-gamma. [33]

There is decreased T-cell response in uremia, marked by 32-40% rate of energy to the intracutaneously administered antigens, [34],[35] which is attributed to uremia and/or dialysis induced defect in the co-stimulatory function of antigen-presenting cells and a persistent inflammatory state of monocytes. [33],[36] Other factors, which might contribute to the decreased immunity, are malnutrition, vitamin D deficiency [37] and hyperparathyroidism. [38]

Features

All studies reported insidious onset of TB with cardinal symptoms of fever, anorexia and weight loss that are usually confused with uremic symptoms. TB presentation in CRF patients is often extra-pulmonary, with percentages varying from 38% up to more than 80% [Table 1], while extra-pulmonary TB accounted for only 4.5% of the cases in the general population. [29],[39] The non-specific symptoms of the extra-pulmonary TB caused delay in the diagnosis of TB, which was observed in several studies.

Tuberculous lymphadenitis and peritonitis were the most reported localizations of the extra-pulmonary TB with only few cases of miliary TB, involvement of the spine (Pott's syndrome), brain and the genitourinary system. Occult or probable TB is a special category that is defined as a strong suspicion of the disease with negative routine and invasive investigations, failure to respond to broad-spectrum antibiotics, and good response to empirical anti-tuberculous therapy. [12] This category comprised 21-50% of the described TB cases in some studies. [4],[9],[27],[30]


   Diagnosis Top


Diagnosis of TB is based on the finding of a smear positive for acid-fast bacilli (AFB), positive culture of M. tuberculosis and typical histopathological findings.

Thus, all efforts should be made to obtain appropriate materials for culture, which should include sensitivity testing. [40] Polymerase chain reaction (PCR) is a sensitive tool to help quick detection of the bacilli in specimens, but is not yet widely available.

The diagnosis of TB might be hampered by a negative purified protein derivate (PPD) (Mantoux) skin test, which was found in some reports in 40-100% of the cases [Table 1]. However, despite the high rate of energy to intracutaneously administered antigens in uremic patients, high rates of positive Mantoux tests in a frequency from 6.1 up to 19% [34],[35] have been found in routine screening of dialysis patients without active or history of TB, and therefore the test should not be abandoned. [31],[34],[35],[41],[42]

Due to the frequent extra-pulmonary presentation and non-specific sympto­matology, a high index of suspicion is required, coupled with a need for invasive procedures, which might include liver-, bone, lymph node and peritoneal biopsies. [12]


   Treatmen Top


Since 1993, the recommended therapy for tuberculosis in the general population has been quadruple therapy consisting of isoniazid (INH), rifampicin (RIF), pyrazina­mide (PZA) and ethambutol (EMB) or streptomycin for 2 months, after which RIF and INH are continued for a total of six months. [43] Extra-pulmonary tuberculosis should be managed according to the same guidelines except for tuberculous meningitis, and children who have miliary or bone/joint tuberculosis; such cases require a minimum of 12 months of therapy. [43]

Several authors have followed stringent approach in the treatment of TB in CRF patients by recommending therapy for 9-12 months (with RIF and INH), and with EMB and PZA added for the first two months. [23],[24],[25],[31] Moreover, some authors cautioned against the use of ethambutol because of the high risk of optic neuritis in uremic patients. [30],[43] In view of the risk of ototoxi­city, the use of streptomycin was proposed to be minimized or avoided in patients with renal failure. [43]

There are some alternative dosage regimens in practice for patients with severe renal failure, on maintenance hemodialysis and on CAPD. [44],[45]

The dosage of rifampicin need not be altered in renal failure, hemodialysis patients and CAPD. [45],[46]

Despite the different metabolic rate of isoniazid in some patients (fast versus slow acetylators), it appears that INH is well tolerated even in slow acetylators with renal failure and as such no dose reduction is necessary. [45] It is recommended to give the dose of INH on dialysis days after dialysis. Side effects of INH include hepatitis, and central and peripheral neurotoxicity. The neurological side effects are preventable by adding pyridoxine in a dose of 100 mg per day. [41],[47]

Ethambutol is usually given in a dose of 15-25 mg/kg BW three times per week after each dialysis. [45],[46] Due to its toxic effects on the optic nerve, visual acuity and color vision should be monitored prior to and regularly during treatment. Serum drug level monitoring is also recommended (two hours post-dose). The committee on adult peritoneal dialysis-related peritonitis treat­ment: 2000 update, did not recommend ethambutol in CAPD patients. [44]

Pyrazinamide is significantly removed by dialysis. [48] It might be given in a dosage of 40 mg/kg BW 3 times per week, 24 hours prior to each dialysis, [45],[46] or 25-30 mg/kg after each dialysis. [46] In CAPD the recom­mended dose is pyrazinamide 1.5 g orally, once a day. [44] Side effects include hepato­toxicity and hyperuricemia.

Only if strictly indicated, streptomycin is given in a dose of 750 mg three times per week 6-8 hours prior to each dialysis, with close monitoring of drug levels. [45]

In cases of multi-drug resistance, second­line medications such as cipro- and ofloxazin, capreomycin, para-amino-salicylic acid (PAS), ethionamide, and cycloserine are available. These drugs have their specific side effects and dose reduction is necessary in severe renal failure.


   Outcome Top


Some early studies, also more recently, reported a high mortality of 17-75% in uremic patients with TB. [3],[4],[5],[8],[9],[20],[27],[29],[30],[31] This was in some instances caused by delay in diagnosis and initiation of therapy due to low index of suspicion with several patients diagnosed post-mortem. The delay of diagnosis and treatment might have lead to deterioration of the nutritional status, which contributed to the death of these patients. [30] In other cases the mortality was apparently not caused by the TB itself or its treatment but by co-morbid conditions.

In contrast to the studies reporting high mortality, others found favorable outcome with practically no mortality, most likely due to early diagnosis and treatment. [12],[15],[18],[19],[23],[24],[25]


   Prophylaxis Top


In view of the high prevalence of tuber­culosis in the dialysis population, several reports have recommended prophylaxis against TB, especially in those patients at high risk of reactivation of TB, such as patients with positive Mantoux-skin test and/or X-rays suggestive of old TB. [23],[24],[25],[31],[34],[41],[42],[49]

Although it is known that there is a high rate of anergy to intracutaneously administered antigens in dialysis patients, routine tuber­culin skin test screening of all patients upon entrance to the dialysis program has been recommended, and, if negative, the test should be repeated with higher strength solution (250 U dose). [41],[42]

The drug of choice for prophylaxis is isoniazid, which can be administered 2-3 times per week under supervision in the dialysis unit at a dose of 15 mg/kg per dose, for a period of six to nine months. [41],[50] The drug should be given together with pyridoxine (100 mg per day).

Tuberculous Peritonitis in Patients on CAPD

The first three cases of tuberculous peritonitis in patients on chronic intermittent peritoneal dialysis were reported in 1982. [51] Although initially thought to be a rare complication of PD, [40],[44] recent reports suggest prevalence of 1.7-1.8%, especially in areas where TB is endemic [30],[54] [Table 2]. The features are often indistinguishable from non-mycobacterial peritonitis, including neutrophil pre-domi­nance of the PD-fluid, [30],[49],[52],[54] which is usually not seen in other forms of tuber­culous peritonitis. [55] The diagnosis should be suspected when a case of peritonitis is not responding to appropriate antibiotic treatment. [44] Unfortunately, the direct AFB smear is positive only in a small minority of the cases [Table 2], and cultures take several weeks to yield a positive result. Therefore, one has to proceed with peritoneal biopsies, or, if not feasible, with empirical treatment. Several reports indicate that the catheter does not need to be removed in all cases [Table 2]. In some instances the TB peri­tonitis is probably not due to re-activation of a latent infection, but to contamination of PD fluid. [30]

Therapeutic aspects have been discussed above (see under treatment).

Infection by Non-Tuberculous Mycobacteria (NTM) (also called a specific Mycobacteria or Mycobacteria other than Tuberculosis; MOTT)

There is a worldwide increase in infections with non-tuberculous Mycobacteria, due to the emergence of the human immuno­suppressive virus (HIV)-epidemic and other factors such as immunosuppressive therapy, malnutrition, and protracted treatment with broad-spectrum antibiotics. These non­tuberculous mycobacteria are ubiquitous organisms, living in soil, water, and dust. Infections with these organisms, in particular group IV (the rapidly growing Mycobacteria, including M. fortuitum and M. chelonae) have been reported in patients on peritoneal dialysis, causing exit site infections and peritonitis, [56],[57],[58],[59],[60],[61],[62],[63],[64] and more rarely, in hemodialysis patients. [65],[66],[67],[68],[69],[70] These infections are often, but not always, due to contaminated water or dialysis fluid, or, in cases of hemodialysis, by infected dialyzers. [67],[71]

The features of peritonitis due to non­tuberculous mycobacterium peritonitis are indistinguishable from non-mycobacterium peritonitis, including neutrophil pre­dominance of the PD-fluid, but are culture negative, and fail to respond to standard peritonitis therapy. In these cases, one should request acid-fast stain of the PD­fluid and Mycobacterium culture, with precise identification and sensitivity testing, as these are essential for optimal manage­ment. Rapidly growing mycobacteria are usually resistant to conventional antituber­culous drugs, and treatment for this group should include clarithromycin and amikacin. [72] Other mycobacteria need different treatment protocols. [72] In cases of such peritonitis, catheter removal seems to be necessary in nearly all cases. [57],[58],[59],[60],[61],[62],[64] A recent review on the topic of non­ tuberculous mycobacterial peritonitis has been published by Yombissi et al. [64]


   Conclusion Top


The conclusion from these observations is that there is an increased prevalence of TB among CRF patients. The prognosis is very much dependent on early diagnosis and treatment. Nephrologists should therefore be aware of the unusual presentation and localization, and include TB in the diffe­rential diagnosis of any patient having non­specific symptoms like anorexia, fever, and weight loss.

All efforts should then be made, including invasive investigations, to reach an early diagnosis, as this determines the outcome.

However, persistently negative investiga­tions, in the face of strongly suspected diagnosis, especially in endemic areas, justifies an empirical trial with anti-tuber­culous medications.

 
   References Top

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Correspondence Address:
Magdi Hussein
Head, Nephrology and Dialysis Unit, Al-Hada Armed Forces Hospital, P.O. Box 1347, Taif
Saudi Arabia
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