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Tuberculosis as we know it is a chronic, contagious, infectious disease that attacks our lungs. Apart from pulmonary tuberculosis there are also spinal tuberculosis, meningeal tuberculosis as well as the main focus of this assignment, renal tuberculosis. According to MacKenzie (2018:620) renal tuberculosis usually begins in one kidney and then it progresses towards the other kidney. Renal tuberculosis makes itself known through the bladder irritation that is caused and are at first always mistaken for cystitis.


According to Eastwood (2001:1307) renal tuberculosis, like other forms of tuberculosis, are caused by members of the Mycobacterium tuberculosis group. M. tuberculosis, the human tubercle bacillus, is the most common organism that causes renal tuberculosis but M. bovis, the bovine tubercle bacillus is also a major factor in causing tuberculosis (Eastwood, 2001:1307).


According to Chijioke (2001:107) the pathophysiology of tuberculosis of the kidneys starts with the first localization of tubercle bacilli in the cortex of the glomerus and this causes stress that ultemately leads to a change in the cell morphology. Krishnamoorthy et al,. (2008:371) is of opinion that the change in cell morphology are called granulomas and they can remain static for a 10-15 years. The presence of tubercle bacilli also causes faster protein synthesis and increased growth of normal glomerular cells as well as the penetrating blood borne cells (Chijioke, 2001:107). This infection can remain in the renal parenchyma without spreading and can result in many forms of glomerulonephritis (Chijioke, 2001:107). According to Sankhe (2014:67) this is the stage where renal tuberculosis occurs as a result of regrowth after dormancy. Sankhe (2014:67) is of opinion that if, at this stage, the infection is not under control or not managed correctly yet, and the hosts’ immune system is diminished, the organism will enter the fluid in the tubular cavity. Further distribution of the bacilli to the medulla and tissues of the pyramid takes place. This causes papillitis that expand into the proximal loop of Henle and this leads to papillary necrosis (Shankhe, 2014:68). It can also lead to the existance of frank cavities that forms abscesses and this leads to the overall scarring of the renal parenchyma (Krishnamoorthy et al,. 2008:372). Krishnamoorthy et al,. (2008:372) also states that together with progression comes formation of lesions in the renal cortex and this results in strictures at the infundibular and pelvi-ureteric junction. This disease can lastly also expand into the collecting system and this results in bacilluria. Renal tuberculosis result in a kidney that does not function as it should, with a large percentage of calcification over the entire area of the kidney and this ultimately leads to renal failure (Krishnamoorthy et al,. 2008:373).

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Clinical manifestations

The greater part of symptoms of renal tuberculosis present in the urine, thus the fact that renal tuberculosis is mostly mistaken for cystitis (Sankhe et el., 2014:68). According to Macalpine, (1935:406), the kidneys will appear damaged in approximately 15% of cases of renal tuberculosis, in all the other cases, this only looks like the bladder that is problematic. Presenting symptoms if renal TB is haematuria, dysuria, nocturia, pyuria and frequency (Malcalpine, 1935:406). Other symptoms that occasionally occur is flank, back and suprapubic pain. It can also be associated with lower back pain and suprapubic pain (Eastwood, 2001:1307). These symptoms usually refer to bacterial cystitis and are thus treated with antibacterial treatment (Macalpine, 1935:406). Only when these antibacterial treatments are not successful, further investigations are done and this only when renal TB is found. Usual symptoms of pulmonary TB like malaise, weight loss and low grade fever are not seen with renal TB (Macalpine, 1935:406). When there is pain present in a kidney, it will not necessarily be the affected kidney. The double responsibility that the healthy kidney has now, can also cause pain (Macalpine, 1935:406).


According to John (1956:102) the triple-drug therapy for renal tuberculosis is made up of 1 g Streptomycin twice a week, 100 mg. Isoniazid eight hourly, and 5g. Sodium Aminosalicylic Acid eight hourly. This need to be given simultaneously and without any interruption for one year. It is of utmost importance that there is no relapse and that this medication is finished. Furthermore, Eastwood (2001:1313) added that a short-course drug regimens are effective when it comes to all kinds of tuberculosis. Usually the following four drugs that shown to be very effective in destroying all the tubercle bacilli: Rifampicin, Isoniazid, Pyrazinamide, and Streptomycin. This treatment is only given for 2 months. After this there will be 4 months were only Rifampicin and Isoniazid are given, and this is to demolish the remaining bacilli that might show any signs of resistance. Direct supervision of this therapy should be ensured because of the fact that failure to comply can cause resistant bacilli (Eastwood, 2001:1313). It is of utmost importance that the course must be finished, otherwise resistant bacilli will be the result.


According to Eastwood (2001:1313) the clinical manifestations of renal tuberculosis imitate the symptoms of other kidney infections. This means that diagnostic awareness can prevent unnecessary death. Diagnosis is extremely difficult, but development in nucleic acid-based bacteriological tests are improving at a very fast rate (Eastwood, 2001:1313). Krishnamoorthy (2008:270) is of opinion that renal tuberculosis is a very common condition but also very difficult to manage due to its various ways of presentation. It is thus of utmost importance that a high grade of suspicion would lead to faster diagnosis and this will lead to a decrease in number of deaths (Krishnamoorthy et al,. 2008:369).

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