Biochemistry Lecture Notes - Uremia: Background, Pathophysiology, Etiology

Background

Uremia is a clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities, which develop in parallel with deterioration of renal function. The term uremia, which literally means urine in the blood, was first used by Piorry to describe the clinical condition associated with renal failure.

Uremia more commonly develops with chronic kidney disease (CKD), especially the later stages, of CKD, but it also may occur with acute kidney injury (AKI) if loss of renal function is rapid. As yet, no single uremic toxin has been identified that accounts for all of the clinical manifestations of uremia. A number of toxins, such as parathyroid hormone (PTH), beta2 microglobulin, polyamines, advanced glycosylation end products, and other middle molecules, are thought to contribute to the clinical syndrome.

Read more: Biochemistry Lecture Notes - Uremia: Background, Pathophysiology, Etiology

Source: Medscape

Biochemistry Lecture Notes - Azotemia: Background, Pathophysiology, Etiology

Background

Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL, and the normal range for serum creatinine is 0.7-1.4 mg/dL.

Each human kidney contains approximately 1 million functional units known as nephrons, which are primarily involved in urine formation. Urine formation ensures that the body eliminates the final products of metabolic activities and excess water in an attempt to maintain a constant internal environment (homeostasis). Urine formation by each nephron involves 3 main processes, as follows: 

• Filtration at the glomerular level 
• Selective reabsorption from the filtrate passing along the renal tubules 
• Secretion by the cells of the tubules into this filtrate 

Perturbation of any of these processes impairs the kidney’s excretory function, resulting in azotemia.

Read more: Biochemistry Lecture Notes - Azotemia: Background, Pathophysiology, Etiology.

Source: Medscape