Brothers Lecture 2

Renal Pathophysiology: Part 2

• Lecture Outline: This lecture covers systemic blood pressure and its influence on glomerular filtration rate (GFR), hormonal regulation of renal perfusion, types of kidney injury, and urine analysis for renal diseases. Learning objectives are included to help students further understand the intricacies involved.

Learning Objectives

• Discuss the renin-angiotensin-aldosterone system (RAAS), atrial natriuretic peptide (ANP), and pressure natriuresis in controlling intravascular volume.
• Describe components of a urinary dipstick.
• Compare and contrast the three main types of acute kidney injury (AKI): prerenal, intrinsic, and postrenal.
• Apply urine analysis findings to clinical case scenarios.

Systemic Blood Pressure & Kidney Function

• Systemic blood pressure directly affects GFR. An increase in blood pressure leads to increased filtration and urine output, reducing blood volume. Conversely, decreased blood pressure has the opposite effect.
• Blood pressure regulation involves both intrinsic and extrinsic mechanisms.
• Intrinsic mechanisms, like the juxtaglomerular apparatus (JGA), autoregulate blood pressure and GFR, automatically. The JGA includes macula densa cells and juxtaglomerular cells.
• Extrinsic mechanisms, include systemic blood pressure, antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and aldosterone.

Regulation of Kidney Function (Intrinsic & Extrinsic)

• Extrinsic mechanisms (outside the kidney) include systemic blood pressure, ADH, ANP and aldosterone.
• Intrinsic mechanisms (inside the kidney) are exemplified by the JGA, and the RAAS.
• Decreased blood pressure triggers the JGA to release renin, initiating the RAAS, which results in salt and water retention, increasing blood pressure.

Renin-Angiotensin-Aldosterone System (RAAS)

• The renin-angiotensin-aldosterone system (RAAS) is a key hormonal system for regulating blood pressure and fluid balance.
• Low blood pressure trigger renin release, activates cascade, forming angiotensin II.
• Angiotensin II causes vasoconstriction and stimulates aldosterone release from the adrenal glands.
• Aldosterone promotes sodium and water reabsorption in the kidneys, increasing blood volume and increasing blood pressure.

Anti-Hypertensives

• Various medications are used to treat hypertension, including ACE inhibitors (ACE-Is) and Angiotensin Receptor Blockers (ARBs).
• Renin inhibitors are another class of drugs used to treat hypertension.

Urine Analysis and Renal Diseases

• Urinalysis: Examines physical (color), chemical (dipstick), and microscopic properties of urine for diagnostics.
• Dipstick Test: Screens for key elements like glucose, protein (albumin), blood, ketones, pH, specific gravity, nitrites, and leukocytes. Values and inferences about diseases can be found from these tests.
• Urine Composition: Waste products like urea and uric acid are excreted. Excesses of other materials can also be detected.
• Urine Sediment: Microscopy analysis determines types and quantity of cells and casts to pinpoint the disease.
• Classification of AKI (Acute Kidney Injury):
  • Prerenal AKI: Initiated by factors in front of the kidney, such as low blood pressure.
  • Intrinsic AKI: Results from intrinsic damage to the kidney tissue.
  • Postrenal AKI: Caused by an obstruction of urine flow past the kidney.

Hormonal Regulation of Volume Balance

• Hormones like ANP and RAAS function as counterbalancing systems in fluid and volume regulation.

• ANP: Released in response to increased blood volume, promotes sodium and water excretion, and vasodilation.

• RAAS: Activated in response to decreased blood volume, resulting in sodium and water retention and vasoconstriction.

Clinical Applications

• Case studies are used to illustrate how urine analysis findings help diagnose and manage renal diseases. Information helps to understand likely diagnoses and how to identify them.