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

Current Approaches for the Detection of Acute Kidney Injury

Acute kidney injury (AKI) is a recognized complication in hospitalized patients. A report in 2009 from National Confidential Enquiry into Patient Outcome and Death (NCEPOD) suggested that AKI was frequently undetected in hospital patients thus contributing to patient morbidity and mortality. Clinical guidelines for recognition and treatment for acute kidney injury were published by NICE (the National Institute for Health and Care Excellence) in 2013 and reported an associated mortality with AKI of more than 25–30%. This guideline also recognized the prevalence of AKI in the primary care population in patients with or without acute illness. NICE also recognized the impact of AKI on healthcare resources, with costs (excluding those in the community) of £434–620 million per year, more than that associated with breast, lung and skin cancer combined

AKI is characterized by an acute loss of the kidney’s excretory capacity leading to accumulation of waste products such as urea and creatinine, and decreased urine output. It is associated with rapid decline in glomerular filtration rate and increases in potassium, phosphate and hydrogen ions. It has varied causes and may be secondary to a non-renal event, thus may be common in hospitalized patients and critically ill patients. It may go undetected in primary care as it can occur without any symptoms. There are associations between co-morbidities, current medications, acute illness and AKI resulting in the high morbidity associated with the condition and the impact on healthcare resources.

Read more: Current Approaches for the Detection of Acute Kidney Injury

Source: cli-online