EXAM2 WK1

Page 1: Kidney Function and Blood Flow

Nephrons: Functional units of the kidney; approximately 800,000 to 1,000,000 per kidney. They cannot regenerate and decrease by about 10% each year after age 40.
Glomerulus: A capillary bed where filtration occurs; it initially filters out everything but selectively reclaims necessary substances afterward.

Bowman’s Capsule: Initial site where filtered fluid is collected.
Glomerular Filtrate: Plasma without proteins; consists mostly of non-protein solutes with concentrations similar to plasma.

GFR Determination:
1. Hydrostatic and colloid osmotic forces across capillary membranes.
2. Capillary filtration coefficient (Kf) - product of capillary permeability and surface area.
Normal GFR: 20% of renal plasma flow.

Increased Hydrostatic Pressure: Elevated glomerular capillary pressure raises GFR.
Regulatory Variables:
1. Arterial pressure
2. Afferent arteriolar resistance
3. Efferent arteriolar resistance
Physiological Regulators:
- Strong sympathetic nervous system activation causes renal vasoconstriction, reducing blood flow and GFR.
- Angiotensin II: Vasoconstricts efferent arterioles to maintain GFR.

Juxtaglomerular Complex:
- Macula Densa Cells: Senses NaCl changes in the distal tubule.
- Juxtaglomerular Cells: Located in arteriolar walls; release renin affecting blood pressure and GFR.
Blood Flow Regulation: Any change in BP could lead to changes in GFR without autoregulation, emphasizes importance of renal control.

Kidney Stones: Cause increased pressure within Bowman’s capsule affecting filtration.
Hydrostatic Pressure Effect: Hydrostatic pressures combined with colloid contribute to changes in GFR, affecting urine output.

Function: Powerful sodium-retaining hormone; triggers in low blood pressure or extracellular fluid volume due to hemorrhage or excessive salt/water loss.

Stimulates Aldosterone Secretion: More sodium reabsorption.
Constricts Efferent Arterioles: Key in maintaining normal waste product excretion.
Direct Sodium Reabsorption: Increases sodium retention across multiple renal segments (proximal tubules, loops of Henle, distal tubules, collecting tubules).

Source: Secreted by zona glomerulosa cells of adrenal cortex.
Key Functions:
- Manages sodium reabsorption and potassium/proton secretion in renal tubules.
- Stimulates sodium-potassium ATPase in the collecting tubule.
Secretion Triggers: Elevated extracellular potassium, increased angiotensin II levels.

Addison’s Disease: Aldosterone absence; results in sodium loss and potassium accumulation.
Conn’s Disease: Excess aldosterone secretion from adrenal tumors leading to sodium retention and decreased plasma potassium.

Function: Increases water permeability in distal tubules and collecting ducts, aids in water retention.
Secretion Triggers: Released from hypothalamus in response to need for water retention.

Central Diabetes Insipidus: Inappropriate ADH secretion leads to significant water loss, treated with synthetic analogs.
Nephrogenic Diabetes Insipidus: Nephrons cannot respond to ADH; treatment focuses on underlying disorders.
Impairment of Countercurrent Mechanism: Can occur through drug interactions impairing urine concentration ability.

GFR Estimation: Best assessed using inulin clearance; neither reabsorbed nor secreted.
Creatinine Clearance: Commonly used proxy for GFR estimation.
PAH Clearance: Used to estimate renal plasma flow due to almost complete clearance from plasma.

Definition: Calculated by dividing GFR by renal plasma flow; indicates fraction of plasma that filters through glomerular membrane.

Azotemia: Elevated blood urea nitrogen and creatinine levels; decreased GFR.
Prerenal Azotemia: Decreased GFR due to kidney hypoperfusion without parenchymal damage.
Postrenal Azotemia: Obstruction in urine flow below the kidneys.
Uremia: Elevated blood urea nitrogen and creatinine linked to clinical outcomes; renal failure causing systemic manifestations.

Nephritic Syndrome: Characterized by blood in urine, moderate proteinuria, azotemia, edema, and hypertension.
Nephrotic Syndrome:
- Proteinuria: > 3.5g/day due to increased glomerular permeability to proteins.
- Hypoalbuminemia: Resulting from prolonged heavy protein loss, decreasing osmotic pressure.
- Edema: Caused by loss of colloid osmotic pressure, activating renin-angiotensin system and promoting fluid retention.
- Hyperlipidemia: Mechanism unclear; may be due to contrasts in protein levels.
- Lipiduria: Increased permeability to lipoproteins.

Acute Pyelonephritis:
- Bacterial infection of urinary tract; most commonly E. coli, known for acute pain and systemic infection signs.
- Results in dysuria and turbid urine due to pus.
Chronic Pyelonephritis: Recurrent infections lead to kidney scarring and potentially renal insufficiency.

Adverse Reactions: Related to various drugs, e.g., synthetic penicillins and NSAIDs.
Mechanism: Can cause immune-mediated tubular injury.

Malignant Hypertension: Vascular injury evokes RAAS activation; angiotensin II constricts intrarenal blood vessels, causing a vicious cycle of increased blood pressure.
Diabetic Nephropathy: Associated with structural damage in diabetic individuals; includes glomerular and renal vascular lesions, leading to renal failure.