Sarcoidosis is an inflammatory condition of uncertain etiology characterized by the presence of noncaseating granulomas involving multiple organs. The disease is now recognized as a member of a large family of granulomatous disorders and has been reported from all parts of the world. Current evidence points to genetic predisposition and exposure to yet unknown transmissible agent(s) and/or environmental factors as etiological agents [21]. The lung is most commonly and usually the first site of involvement, and the inflammatory processes extend through the lymphatics to the hilar and mediastinal nodes [22]. The lung is involved in more than 90 % of cases. Pulmonary sarcoidosis starts as diffuse interstitial alveolitis, followed by the characteristic granulomas. Granulomas are present in the alveolar septa as well as in the walls of the bronchi and pulmonary arteries and veins. The center of the granuloma contains epithelioid cells derived from mononuclear phagocytes, multinucleated giant cells, and macrophages. Lymphocytes, macrophages, monocytes, and fibroblasts are present at the periphery of the granuloma [23]. Sarcoidosis represents a challenge to clinical investigation because of its unpredictable course, uncertain response to therapy, and diversity of potential organ involvement and clinical presentations [24]. The diagnosis is based on a compatible clinical and/or radiological picture, histopathological evidence of noncaseating granulomas in tissue biopsy specimens, and exclusion of other diseases capable of producing similar clinical or histopathological appearances. Even microscopically, the noncaseating granulomas are not specific [21]. Infection by mycobacterial species other than Mycobacterium tuberculosis frequently leads to the production of noncaseating granulomas [25]. The condition is underdiagnosed in some areas. However, owing to the increasing awareness, it is being diagnosed more frequently than a few decades ago [26].

The disease runs a benign course with spontaneous remission of the activity though some degree of residual pulmonary function abnormality persists. Only a minority of patients develop complicated disease that may lead to blindness, renal failure, liver failure, and heart involvement.

Corticosteroids remain the mainstay of treatment. Treatment under close clinical monitoring should be tailored to suit the needs of the individual patient hence the need to evaluate disease activity [26].

Advanced age, the presence of pulmonary symptoms, the presence of parenchymal lesions on chest radiograph, a previous history of treatment with corticosteroids, and the presence of extrathoracic involvements at the time of detection are possible prognostic factors in patients with sarcoidosis [27]. The mode of onset and the extent of the disease are also related to prognosis. An acute onset with erythema nodosum or asymptomatic bilateral hilar lymphadenopathy usually heralds a self-limiting course, whereas an insidious onset, especially with multiple extrathoracic lesions, may be followed by relentless, progressive fibrosis of the lungs and other organs

Pneumocystis carinii (jiroveci) pneumonia (PCP) is a condition that may be endemic or epidemic. It is caused by Pneumocystis carinii, which was considered as a protozoon and recently as a fungus. The condition is common in premature infants, debilitated children, and in other immunocompromised conditions, particularly the acquired immune deficiency syndrome (AIDS), but it is also seen in congenital immunodeficiency and in patients who are receiving chemotherapy and corticosteroids. It remains a significant cause of morbidity and mortality in human immunodeficiency virus and nonhuman immunodeficiency virus-associated immunosuppressed patients [28]. It is the most common infection in AIDS patients, and it remains an important cause of morbidity and mortality [29]. The introduction of highly active antiretroviral therapy in industrialized nations however has led to dramatic declines in the incidence of AIDS-associated complications, including PCP. In the developing countries, no decline has occurred [30]. Transmission is usually airborne. The pathological changes are predominantly in the lungs with an inflammatory reaction consisting of plasma cells of variable amount, monocytes, and histiocytes. This disease has also been reported in immunocompetent patients, and in this case the presentation is more closely resembling the disease of immunocompromised patients other than AIDS patients [31, 32]. The diagnosis is currently established through identification of the organisms in bronchial secretions obtained by bronchoalveolar lavage or bronchial washings [33]. Gallium-67 is an important imaging modality that helps in the diagnosis and evaluation of the activity of the disease.

Interstitial pulmonary fibrosis, a sometimes fatal condition, is characterized by parenchymal inflammation and interstitial fibrosis. The pathological changes start with alveolitis; this is followed by derangement of the alveolar-capillary units, leading to the end stage of fibrosis. There is a correlation between the inflammatory activity and the amount of gallium-67 activity in the lungs [34].

Acute pyelonephritis is a common medical problem. The diagnosis and management of this condition is complex. Patients initially diagnosed with pyelonephritis typically exhibit symptoms and laboratory evidence suggesting infected urine, with signs referable to upper urinary tract infection. However, no consistent set of signs and symptoms are sensitive and specific for this diagnosis. Symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day. Symptoms of lower UTI may or may not be present. These include dysuria; urinary frequency, hesitancy, and urgency; gross hematuria; and suprapubic discomfort, heaviness, pain, or pressure. Additionally, flank pain and tenderness, unilateral or sometimes bilateral, are present. Fever is not always present. When present, it is not unusual for the temperature to exceed 103 °F (39.4 °C). Rigor, chills, malaise, and weakness may be present. Anorexia, nausea, vomiting, and diarrhea may also be present. Most patients have significant leukocytosis, pyuria with leukocyte casts in the urine, and bacteria on a gram stain of unspun urine.

Many conditions and clinical situations are associated with an increased risk of pyelonephritis. Table 4.2 lists common risk factors.

Pyelonephritis is significantly more common in females (higher in white than in black) compared to males. Approximately 10–30 % of women develop a symptomatic UTI at some point in their lives.

Acute pyelonephritis is a bacterial infection of the kidney with acute inflammation of the pyelocaliceal lining and renal parenchyma centrifugally along medullary rays. This can occur by more than one way. Most often it occurs because of ascending infection from the lower urinary tract (Fig. 4.4). The initial colonization of the walls of the ureter is in areas of turbulent flow which leads to paralysis of peristalsis. Dilation and functional obstruction result in subsequent pyelonephritis. Another way is by direct reflux of bacteria. Hematogenous spread to the kidney by gram-positive and less likely by gram-negative organisms is the third way that can occur. This has become less prevalent since the advent of rapid use of antibiotics. Little or no evidence supports lymphatic spread.

Grossly, the kidney is enlarged and edematous. The cut surface may show small abscesses in the cortex, and more often there are wedge-shaped purulent areas streaking upward from the medulla, with normal areas of the kidney tissue intervening in between infected zones (Fig. 4.5). Frequently, the pelvis and calyces are inflamed and dilated. In severe infection, renal papillary necrosis may be present.

Microscopically, there is intense inflammation, with infiltration of polymorphonuclear leukocytes throughout the interstitial tissue and abscess formation. There is destruction of the tubules, but the glomeruli and blood vessels are often unaffected. The disease remains essentially focal in character, with areas of normal tissue. Following treatment and removal of predisposing factors such as obstruction, healing may occur, leaving coarse scars which stretch from the medulla to the capsule of the kidney.

Chronic pyelonephritis is a chronic condition affecting the pelvis and parenchyma and resulting from recurrent or persistent renal infection. It occurs almost exclusively in patients with major anatomic anomalies, including urinary tract obstruction, struvite calculi, renal dysplasia, or, most commonly, vesicoureteral reflux (VUR) in young children. Grossly, the kidney shows normal areas alternating with zones of scarring. Wedge-shaped scars can be seen on the subcapsular surface of the kidney. The appearance differs, depending on the presence or absence of obstruction. Chronic pyelonephritis in the presence of intra- or extrarenal obstruction shows dilation of the pelvocalyceal system and sometimes peripelvic fibrosis. If no obstruction is present, the pelvic change is in the form of peripelvic fibrosis rather than dilation (Fig. 4.6).

Microscopically, the scarred areas show changes in the interstitium and tubules. The interstitial tissue shows infiltration by predominantly lymphocytes and plasma cells. The tubules become atrophic and may collapse (Fig. 4.7). The glomeruli may be normal in some cases, while in others periglomerular fibrosis is present.