Saudi Journal of Kidney Diseases and Transplantation

: 2009  |  Volume : 20  |  Issue : 2  |  Page : 270--273

Concurrent Kaposi's sarcoma, tuberculosis, and allograft dysfunction in a renal transplant patient

Fuad Alshaebi, Bappa Adamu, Waleed Alghareeb 
 Nephrology Division, Department of Medicine, King Fahad Medical City, Riyadh, Saudi Arabia

Correspondence Address:
Fuad Alshaebi
Department of Medicine, King Fahad Medical City, P.O. Box 59046, Riyadh 11525
Saudi Arabia


The major long-term complications of renal transplantation (RT) include cardio­vascular disease, opportunistic infections, malignancies, and chronic allograft nephropathy. Long­term complications are generally considered as those occurring more than 1 year post trans­plantation; however, some of the complications can occur earlier. We present a 58-year-old man who presented with multiple complications of RT concurrently and relatively early post trans­plantation including Kaposi«SQ»s sarcoma, tuberculosis and allograft dysfunction.

How to cite this article:
Alshaebi F, Adamu B, Alghareeb W. Concurrent Kaposi's sarcoma, tuberculosis, and allograft dysfunction in a renal transplant patient.Saudi J Kidney Dis Transpl 2009;20:270-273

How to cite this URL:
Alshaebi F, Adamu B, Alghareeb W. Concurrent Kaposi's sarcoma, tuberculosis, and allograft dysfunction in a renal transplant patient. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2023 Feb 4 ];20:270-273
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Full Text


Renal transplantation (RT) is currently the standard of care for the treatment of end- stage renal disease. However, the post-transplanta­tion period is hampered by many potential complications which can lead to morbidity and/or mortality.

The three most commonly defined causes of death in the late post transplant period are cardiovascular disease (CVD), infection, and malignancy. [1] Chronic allograft dysfunction on the other hand accounts for 50% of allograft loss after the first year post transplant. These complications usually occur in the late post­transplantation period, but can present rela­tively early.

There have been reports of co-existence of opportunistic infections and malignancies, [2],[3],[4],[5],[6] as well as more than one opportunistic infection in the same patient. [1] We report the occurence of opportunistic infection, malignancy, chronic allograft dysfunction, and cardiovascular di­sease all co-existing in the same patient, rela­tively early in the post-transplantation period.

 Case Report

A 58-year-old Saudi man with a history of end-stage renal disease secondary to diabetic nephropathy received live unrelated kidney transplantation abroad 8 months prior to pre­sentation to our center, and he was followed up at peripheral local hospital. His immuno­suppressant regime consisted of cyclosporine 100 mg BID, mycophenolate mofetil 500 mg BID and prednisolone 5 mg QD.

The patient presented with a 3-month history of intermittent fever and generalized non-pru­ritic, painless pigmented skin lesions, first no­ticed on the limbs then other parts of the body. He also complained of headaches and neck pain with restricted neck movements for 1 month earlier. He had been unable to walk without support for about 3 weeks prior to pre­sentation. However, there was no history of a significant weight loss. His past history was remarkable for a single vessel ischemic heart disease stented 4 years prior to transplantation. The review of the systems was otherwise unre­markable.

On examination, the patient was febrile (38.2°C) and looked sick. His blood pressure (BP) was 175/76 mmHg. Skin examination was remarkable for nodular, violaceous skin lesions [Figure 1] that involved both upper and lower limbs, trunk, scalp, ear lobes, face, and hard palate, dull percussion notes on the left lung base with decreased intensity of breath sounds, neck stiffness with a negative Kernig's sign, and mild ankle edema. However, there was no significant peripheral lymphadenopathy, abnor­mal heart sounds or abnormal nervous system examination.

Laboratory investigations included cerebro­spinal fluid biochemistry that was normal and stain negative for fungi and acid fast bacilli. Tuberculin skin test was negative. Urinalysis showed protein 1+ and microscopy was nor­mal. The complete blood count revealed mild microcytic hypochromic anemia with hemo­globin 11 g/dL and lymphopenia of 0.57 x 10 9 /L (1.5-3.5). Abnormal biochemical blood investigations included creatinine: 183 µmol/L, urea: 14.3 mmol/L, and albumin: 21 g/L. How­ever, electrolytes, liver enzymes, bilirubin, cardiac enzymes, and lipid profile were all within normal limits. Cyclosporine through level was 127 ng/mL. Serology tests for heap­titis B and C, HIV, Ebstein-barr virus and cytomegalovirus were all negative.

Renal allograft ultrasound revealed a normal sized and echotexture kidney. Doppler ultra­sound revealed low perfusion in the transplan­ted kidney with stenosis at the transplant anas­tomotic site estimated to be less than 60%. Re­sistivity index was 0.87 and peak systolic velocity of 580 cm/second.

Chest x-ray [Figure 2] showed opacification of the left hemithorax with decreased volume and fibrotic changes as well as pleural thickening/effusion. The right lung field showed di­ffuse interstitial opacities. High resolution CT scan [Figure 3] showed consolidation and cavi­tation involving the left upper and lower lobes. Patchy nodules were noted on the right in addition to bilateral pleural and mild pericar­dial effusion. X-ray of the cervical spine re­vealed degenerative changes involving C2-6 and bilateral cervical ribs.

Skin biopsy [Figure 4] was consistent with Kaposi's sarcoma (KS). Electrocardiogram (ECG) showed nonspecific ST-T changes.

Sputum was positive for acid fast bacilli and MTB complex by polymerase chain reaction. Culture yielded mycobacterium tuberculosis (TB) sensitive to isoniazid (INH), rifampicin, pyrazinamide and ethambutol. The patient was placed on all these anti-Tubercular drugs. He improved clinically, with partial regression of the KS lesions, gradual ambulation, and im­provement in renal function with a decrease of s. creatinine to 140 µmol/L at the time of discharge.


The post transplant period is traditionally divided into early and late transplant periods. Most authors use the 1- year limit to define the onset of late post transplant period. [1]

TB can occur anytime post-transplantation, though in most instances it develops in the first few months when immunosuppression is maxi­mal; hence, it is considered as an early period opportunistic infection. [7] Renal transplant pa­tients are at increased risk of disseminated TB (40-60% compared to 0.6-1.4% in the general population) due to immunosupression. [8] It is di­fficult to exclude dissemination in our patient, especially with the finding of pericardial effu­sion, although this could be due to hypo­albuminemia. The treatment of post transplant TB is essentially the same as in the general population. [8]

The presentation of KS in our patient is rela­tively early considering the published median interval of about 30 months was reported. [9],[10] Since the recognition of human herpes virus type 8 (HHV8) in KS lesions in an AIDS pa­tient in 1994, [11] it is accepted that HHV8 plays a key role in the pathogenesis of KS. The treat­ment of post transplant KS varies between institutions, but there is a consensus that immunosuppressive medications should be re­duced. [12] More recently, there are several re­ports of the effectiveness of sirolimus, an antiproliferative agent in the treatment of post transplant KS. [13],[14] However, a study by Bora­ tynska et al suggests that regression of KS is a result of diminished immunosuppression, not the direct antineoplastic effect of sirolimus. [15]

The elevated creatinine in our patient at pre­sentation was multifactorial. He had sonogra­phic evidence of renal artery stenosis although no intervention was contemplated because he had good blood pressure control and renal func­tion improved on medical treatment. The pa­tient also has many of the recognized risk fac­tors for chronic allograft dysfunction namely diabetes mellitus, uncontrolled hypertension, proteinuria, and hypoalbuminemia. [1] Poor com­pliance is also a possibility, as this patient did not come with a medical report from his pri­mary physician and failed to come for follow­up after discharge despite contacts by phone. Poor compliance is also a recognized risk fac­tor for chronic allograft dysfunction. [1] In addi­tion to uncontrolled hypertension, the patient also had diabetes and pre-transplant ischemic heart disease as risk factors for cardiovascular disease. The peculiarity of his presentation is the concurrence Kaposi's sarcoma and TB concurrently and relatively early post trans­plantation, which suggests over immunosu­ppression. Despite these complications, the pa­tient responded to treatment and was dis­charged from the hospital.


We are grateful to Dr. Ihsan Housaini who provided the pathology slides.


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