Table 1.

Summary table for sarcoidosis

Etiology	Exact etiology remains elusive Likely multifactorial ○ Environmental exposure ○ Infectious agents ○ Immunogenetic ■ Major histocompatibility complexes ■ T-cell abnormalities ■ T-cell receptor reactivitiy [1] Renal involvement either due to hypercalcemia/hypercalcuria from increased calcitriol production, or from direct granulomatous infiltration. Underlying etiology remains the same for all organs [18].
Incidence	In the United States, the incidence of any form of sarcoidosis among black Americans is about 35.5 cases per 100,000, which is about three times that of white Americans, which is 10.9 per 100,000. [1] Incidence of renal involvement in sarcoidosis is unknown. There have been less than ten case reports of pseudotumorous granulomatous infiltration of the kidneys [18–22].
Gender Ratio	Predilection for females developing any form of sarcoidosis Variable gender ratio, tends to be around 2:1 females to males [1]. Uncertain if there is a specific gender predilection for renal involvement in sarcoidosis [18].
Age Predilection	Black Americans: the peak incidence of sarcoidosis is in the fourth decade for both men and women. Other ethnic and racial groups, the age of onset is variable. All cases considered, the majority present between the ages of 10 and 40. Young children and the elderly may still present with the disease, likely will be atypical presentation [1–3].
Risk Factors	The lifetime risk of sarcoidosis is in black Americans at 2.4% ○ Black Americans tend to develop more acute, severe disease That of white Americans at 0.85%. ○ Whites may be asymptomatic or have mild, chronic disease. Associations with specific immune-related genes (HLA DR 11, 12, 14, 15, and 17) have been made and seem to confer increased susceptibility. Exposure to hazardous occupational and environmental particulates has been hypothesized to increase the risk. ○ Specific exposures are unknown. People of a lower socioeconomic are more likely to present at more advanced stages because of lack of access to healthcare [1–4].
Treatment	First line treatment for both pulmonary and extrapulmonary manifestations in symptomatic patients is prolonged glucocorticoid therapy Dosing is dependent on the severity of the symptoms and the rate at which they are progressing ○ Usually is initiated at 20–40mg of prednisone daily for moderately severe symptoms ○ 80–100mg daily for severe respiratory, cardiac, neurologic, or ocular disease. Initial therapy lasts for 4–12 weeks depending on response, Maintenance therapy at about half the dose continues for 6–12 months Response to therapy is monitored based on functional status as well as comparative imaging, although there is no standardized way to monitor therapy Methotrexate, azathioprine, leflunomide, and antimalarials are all possible alternatives to those not responding to or intolerant of glucocorticoids [1,4].
Prognosis	The overall mortality from sarcoidosis is less than 5% ○ Stems from pulmonary fibrosis, pulmonary hemorrhage, or arrhythmia secondary to myocardial involvement. Patients who are responsive to treatment and are relapse-free after a year are unlikely to have relapses. Relapses may occur during tapering of therapy or within the first year following cessation of therapy, and chronic low-dose steroid therapy may be necessary [1]. In renal sarcoidosis, if the kidney function has been affected by the fibrosis and inflammation, there is less probability of regaining full kidney function. ○ If kidney involvement is extensive, a patient may need dialysis or a transplant [18].
Findings on Imaging	Lungs: ○ Classic radiographic imaging of the chest, may reveal ■ bilateral hilar adenopathy ■ reticular parenchymal opacities [4]. ○ High resolution CT of the chest may reveal ■ nodularity ■ bronchial wall thickening ■ stranding ■ predominance in the middle and apical regions of the lungs Heart: ○ Cardiac MR is valuable for the visualization of ■ scar tissue ■ myocardial inflammation in non-ischemic distributions [15, 16]. Liver and Spleen: ○ Sarcoid manifestations in the liver and spleen are the most common intraabdominally ○ Hepatomegaly and splenomegaly from granulomatous infiltration ○ Hepatic and splenic nodules formed from coalescent granulomata are also potential presentations. ■ The nodules are multiple, well-defined, hypoechogenic on ultrasound, and hypodense on CT [17]. Kidneys: ○ Interstitial nephritis is a possible manifestation ■ May demonstrate a striated nephrogram on contrast-enhanced CT [18, 19] ○ Renal Pseudotumors: ○ May be singular or multiple ○ Unilateral or bilateral. ○ They may be echogenic on ultrasound [22]. ○ Focal, exophytic nodules that may exhibit hypo-, iso-, or hyperdense attenuation on noncontrast CT relative to the normal renal parenchyma, but are hypo-enhancing on contrast-enhanced CT [20–22]. ○ MRI, ■ Poor circumscription of the mass or masses from the renal parenchyma, indicating interstitial infiltration. ■ On unenhanced T1 and T2-weighted imaging, the pseudotumor may be homogenous or slightly heterogeneous, predominately remaining isointense to the surrounding renal parenchyma [20–22]. ■ Following gadolinium-based intravenous contrast, there is less early and delayed enhancement relative to the normal renal cortex on both T1 and T2 imaging, a consistent feature reported in all available case reports that have evaluated these masses by MRI. ○ Whole-body PET using 18F-FDG has demonstrated intense radiotracer uptake by such masses.