Currently, the pathogenesis of HIVAN is still unknown, which is possibly related to the following factors: (1) direct infection of HIV to the kidney parenchymal cells, and then invasion of the renal epithelial cells including visceral epithelial cells and tubular epithelial cells; (2) indirect renal lesions after the coding products of HIV in the blood circulation being absorbed by renal cells; (3) indirect renal lesions caused by the cytokines released from HIV infected lymphocytes and mononuclear cells in the kidney. In addition, it may also be related to gene and environmental factors.

The pathologic changes of HIVAN are characteristic, mainly including enlarged kidney volume, proliferation of epithelial cells, the whole or segmental contraction and collapse of the glomerular capillary wall with obvious podocyte proliteration, apoptosis in the glomerulus and renal interstitium. By light microscopy, the findings of whole collapse of any one glomerulus or segmental collapse in more than 20 % glomerulus should be suspected as the disease. Under an electron microscope, large quantity tubuloreticular inclusion bodies (in 80–90 % HIVAN patients) in endothelial cells and interstitial leukocytes of the glomerulus can facilitate to define the diagnosis.

Including serious albuminuria (above 3.5 g/day), azotemia, water electrolyte imbalance, hematuria by naked eyes, normal blood pressure, normal/enlarged kidney, acute progressive renal dysfunction. The normal blood pressure is characteristically HIVAN.

In the advanced stage of HIV infection, albuminuria occurs (being higher than 1 g/24 h), with increased creatinine. By the diagnostic imaging, the kidney is found enlarged and renal failure with other etiologic factors excluded. The cases with no typical clinical manifestations or ineffective treatment by antiretroviral therapy or other therapies should be performed kidney tissues biopsy to define the diagnosis.

Almost all cases of renal tuberculosis occur secondary to pulmonary tuberculosis, and occasionally secondary to joint tuberculosis, lymphaden tuberculosis and intestinal tuberculosis. The invasion of tubercle bacilli to the kidneys is via 4 routes, blood, urinary tract, lymphatic vessel and direct extension. Blood borne spreading to the kidneys is recognized as the most common transmission route. Blood borne infection of renal TB is mostly simultaneous infections of both kidneys. However, in its progressive process, the severity of renal TB may be more serious in one kidney than the other. Due to the compromised immunity, the conditions may develop rapidly, with possible serious lesions in both kidneys. Pathological examinations have demonstrated that more than 80 % cases have simultaneous infection of both kidneys. But actually, the contralateral lesions are slight and can be self healed. Therefore, the clinical cases of renal TB is mostly unilateral, accounting for about 85 % and the cases of bilateral renal TB account for about 10 %.

Ureter tuberculosis is caused by downward spreading of the homolateral renal tuberculosis. And it can also be caused by the urinary reflux of mycobacterium tuberculosis in the bladder for the retrograde infection.

About 50–70 % of male patients with renal tuberculosis sustain the complication of reproductive system tuberculosis. Its occurrence in males originates from the prostate and the seminal vesicle. The condition with the most obvious clinical symptoms is epididymis TB. In the patients with renal TB complicated by reproductive TB, about 40 % have their epididymis tuberculosis occurring before or during the occurrence of renal tuberculosis.

Along with the blood flow, mycobacterium tuberculosis invades the kidney to cause lesions, of which 90 % are located in the cortex and 10 % in the medulla. Cortex tuberculosis infection is self healing. However, in the cases with further progression, the medulla may be involved to form caseous necrosis and tuberculous abscesses. The abscess can penetrate into the kidney calices to cause cavities after the necrotic materials being discharged. The abscess rupture and access of mycobacterium tuberculosis into the urine via the tubules can cause mucosa lesions and ulceration in the kidney calices and pelvis. Subsequently, due to the formation of tuberculous granulation tissue, stenosis of the kidney calices and pelvis occurs with their wall thickened. Calyceal stenosis can cause the infection to involve the other kidney calices and further invade the adjacent renal parenchyma. The primary lesions in the renal parenchyma can also gradually enlarge to cause extensive lesions in the renal parenchyma to form multiple cavities. Therefore, tuberculous pyonephrosis occurs. This type is the most commonly found in the clinical practice. In some patients, if the compromised immunity improves, caseous materials thus are concentrated rather than liquefaction to cause extensive fibrous tissues hyperplasia and calcification, which is known as autonephrectomy or plaster kidney. Although the disease may clinically progress to calcified autonephrectomy, the actual pathological changes are caseous cavities, fibrous atrophy, and mixed hard nodules and calcification. Tubercle bacilli can still exist in the caseous substances.

Ureter tuberculosis often invades the ureteral mucosa, mucosal lamina propria and muscularis. In the early stage, ureteral mucosa is damaged, which leads to ulceration and lumen dilation. Subsequently, due to the formation of tuberculous granulation tissues, the ureteral wall is thickened and rigid, with stenosis and even occlusion. Urethral stenosis commonly occurs most commonly at the ureterovesical junction, followed by the ureteropelvic junction. Its occurrence at the middle segment is rare. The involved ureter can be partially or totally calcified.

Bladder tuberculosis is commonly caused by spreading of renal or ureteral tuberculosis. In the early stage, it is demonstrated to have bladder mucosal congestion, edema, irregular ulcers and (or) granuloma. The lesion begins adjacent to the ipsilateral ureteral opening, and then spreads to other parts to involve the delta or even the whole bladder. In the advanced stage, the lesions invade into the myometrium to cause serious fibroplastic proliferation and scar contraction, resulting in the shrinkage of the bladder capacity to less than 50 ml. It is known as bladder contracture. Bladder fibroplastic proliferation can cause ureteral stenosis or ureteral incompetence to form cave liked lesions. Both can lead to obstruction and urine reflux in the ureters, resulting in hydronephrosis. Ureteral incompetence also allows urine in the bladder flowing upwards to infect the contralateral kidney. In the cases of serious bladder lesions and deep ulceration, the bladder wall can be penetrated to involve the vagina or the rectum, resulting in vesico-vaginal fistula or vesico-rectal fistula.

The main pathological changes of urethral tuberculosis are ulcer and stenosis, which can cause dysuresia and urinary fistula and aggravate the kidney dysfunction.

The patients with renal tuberculosis commonly sustain the symptoms of urgent urination, frequent urination, painful urination and other bladder irritation symptoms, with accompanying hematuria, pyuria, backache, anemia, low grade fever, night sweating, poor appetite, weight loss, fatigue and other systemic symptoms.