No abstract

Once the tubercle bacilli are ingested by alveolar macrophages, they are either destroyed, inhibited, or they may multiply intracellularly. If the bacilli multiply, they may then spread to other organs and systems via lymphatic channels or the bloodstream [4,5]. Although TB is a common disease with a rising incidence even in the developed world, there is still much that is unknown about the less common form known as Miliary TB, including its varied presentation and its complex treatments. Miliary TB remains a diagnostic challenge, as it accounts for less than 2% of all confi rmed cases of TB and up to 20% of all extra-pulmonary TB (EPTB) cases in various clinical studies [6].

Excess production or absorption of oxalate can lead to hyperoxaluria and subsequent kidney injury. While many etiologies of hyperoxaluria have been well studied, diet-induced secondary oxalate nephropathy is a rare cause of renal damage that is still poorly understood. In this report, we present a 71-year-old man who lacked any known risk factors for secondary oxalate nephropathy other than a diet that was unusually high in peanut butter and coffee. The patient developed severe acute kidney injury, which resulted in end-stage renal disease and dependence on hemodialysis. Renal biopsy showed oxalate crystal buildup to be the culprit. It is likely that these cases of diet-induced secondary oxalate nephropathy have a strong genetic component that is yet to be fully understood. As the general public is likely unaware of the significance of dietary oxalate, we believe it is important to quickly identify and educate patients that have relevant risk factors to prevent development of acute or chronic kidney disease.

Background Hypokalemic periodic paralysis is a chronic condition characterized by sporadic attacks of weakness associated with acute hypokalemia. Attacks are typically associated with specific triggers, such as prolonged rest following exercise or consumption of a high-carbohydrate meal. Most commonly, this condition is caused by an autosomal dominant calcium channel mutation, and patients typically have an established family medical history of hypokalemic periodic paralysis. Long-term complications include the development of progressive proximal myopathy. Oral potassium chloride may be considered for the treatment of an acute attack, with administration of acetazolamide or dichlorphenamide as long-term prophylaxis. Nephrologists can play an important role in the recognition and treatment of previously undiagnosed hypokalemic periodic paralysis. Case presentation We summarize the case of a 19-year-old white man who presented to the emergency department with undiagnosed attacks of hypokalemic periodic paralysis, and who reported, at follow-up, improvement in the severity and frequency of attacks with dichlorphenamide. Conclusions This case demonstrates the crucial role nephrologists can play, not only in the diagnosis of hypokalemic periodic paralysis, but also in the ongoing management of this condition. Patients should be advised to regularly follow up with their nephrology team for evaluation due to the risk of developing myopathy.