Question

You have a hypovolemic person (due to dehydration) in Metabolic Acidosis with a history of Hypertension and Chronic Kidney Disease.

Draw or write about what is happening before and during the Pre-Renal and Intra-Renal phases related to their state.

Answer 1

Metabolic acidosis is commonly found in patients with chronic kidney disease ( CKD),and its causes are: impaired ammonia excretion,reduced tubular bicarbonate reabsorption and-insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food.

Acute Kidney Injury(AKI): is a sudden loss of renal function with a consecutive rise in creatinine and blood urea nitrogen (BUN).It is most frequently caused by decreased renal perfusion ( prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drinage( post renal).In AKI,acid base homeostasis,as well as the fluid and electrolyte balance is disturbed,and the excretion of substances,including drugs,within the urine is impaired.The main symptom of AKI is oliguria or anuria,in some cases,polyuria may occur as a result of disturbed tubular reabsorption

Prerenal phase in Acute Kidney Injury (AKI): decreased renal perfusion ( often from hypovolemia) leading to a decrease in Glomerular Filtration rate(GFR),reversible.Which( if proloned or severe) can progress to ischemic acute tubular necrosis (ATN)

Pathophysiology: Decreased blood supply to kidneys( due to hypovolemia,hypotension,or renal vasoconstriction) leads to failure of renal vascular auto regulation to maintain renal perfusion,leads to decreased GFR leads to activation of renin- angiotensin system lead to increased aldosterone release leads to increased reabsorption of Na+,H2O leads to increased urine osmolality leads to secretion of anti diuretic hormone leads to increased reabsorption of H2O and urea.

Creatinin is still secreted in the proximal tulles,so the blood BUN: creatinine ratio increases.

Intra renal phase: intrinsic kidney injury,(often from prolonged or severe renal hypo perfusion).ATN most common due to ischemic/ nephrotoxic injury.

Pathophysiology: Damage to a vascular or tubular component of the nephron leads to necrosis or apoptosis of tubular cells leads to decreased reabsorption capacity of electrolytes ( e.g.,Na+),water,and/ or urea ( depending on the location of injury along the tubular system) leads to increased Na+ and H2O in the urine leads to decreased urine osmolality.