The history of a newborn developing severe renin-induced hypertension is reported. A thrombotic occlusion of the lower a.abdominalis with an ascending thrombus into the left a.renalis caused hypertension according to the two-kidney-one-clip hypertension. High pressure diuresis induced weight loss by polyuria, hyponatremia and hypokalemia by severe renal salt losses. The vicious circle of malignant hypertension was initiated by sodium losses, not sufficiently recompleted by therapy. The full picture of an acute hypertensive renal damage was seen at autopsy in the unclamped kidney.

A 22 year old female was admitted to the emergency department with high fever up to 41,5 degrees C, tachycardia, and arterial hypotension. Clinically, she presented with bilateral pulmonary coarse crackles. Diagnosis on admission was pneumonia with septic shock. Intriguingly, procalcitonin (PCT) was increased early, reaching up to 435 ng/mL, while C-reactive protein levels were only moderately increased, with several days delay. The sepsis was originated from a multi-resistant pseudomonas aeruginosa pneumonia. Remarkably, the course of PCT levels reflected the severity of septic shock in that it paralleled noradrenaline demand. Ten months previously, the patient had been diagnosed with acute disseminated brainstem encephalitis (ADEM), and had received two cycles of intravenous cyclophosphamide. Our case illustrates that PCT is an early marker for sepsis and it indicates that PCT may also be a valuable marker for the severity of sepsis in immunosuppressed patients.

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