When alcohol is consumed at a rapid rate, the point at which most healthy peoples long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for infrequent drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.Chronic alcoholism often leads to a thiamine (vitamin B1) deficiency in the brain, causing Korsakoffs syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernickes encephalopathy (WE). The memory impairment that is pathognomonic to Korsakoffs syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory. Pathophysiology
The pathophysiology of anterograde amnesic syndromes varies with the extent of damage and the regions of the brain that were damaged. The most well-described regions indicated in this disorder are the medial temporal lobe (MTL), basal forebrain, and fornix. Beyond the details described below, the precise process of how we remember – on a micro scale – remains a mystery.
The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms tumor, and renal cell carcinoma, all of which may produce renin. Hypertension secondary to other renal disorders
Chronic kidney disease
Kidney disease / renal artery stenosis –  the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration.Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated. Renal segmental hypoplasia (Ask-Upmark kidney)

Hypertension secondary to endocrine disorders
Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland. The specific mechanism involved is increased release of the "stress hormones", epinephrine (adrenaline) and norepinephrine which increase blood output from the heart and constrict arteries.