Kidney Function and Tubular Reabsorption M3 PP

The movement of substances from the tubular filtrate back into the plasma.

The movement of substances from the plasma into the tubular filtrate.

The process by which the kidneys filter the blood, separating wastes and excess fluids from the blood.

The rate at which the kidneys filter blood.

A decrease in blood flow to the kidneys.

Local substances released in response to injury or stress in the kidneys.

If the efferent arteriole dilates more than the afferent arteriole, GFR increases.

If the efferent arteriole constricts more than the afferent arteriole, GFR decreases.

Angiotensin II causes vasoconstriction of the efferent arteriole, which helps to maintain glomerular filtration pressure by increasing resistance to outflow.

The three major renal tubular processes are filtration, reabsorption, and secretion. Filtration is the movement of fluids and solutes from the blood into the Bowman's capsule. Reabsorption is the movement of substances from the filtrate back into the blood. Secretion is the movement of substances from the blood into the filtrate.

Reabsorption requires energy (ATP) to move substances against their concentration gradient from the filtrate back into the blood.

An important function of the kidneys is to maintain proper fluid balance.

Reabsorption and secretion are essential for maintaining fluid balance.

Kidneys help to regulate blood pressure by adjusting fluid volume.

Kidneys play a significant role in electrolyte balance, ensuring proper function of cells and tissues.

Kidneys filter and remove waste products from the blood, helping to maintain homeostasis.

The kidneys' primary function is to create concentrated or diluted urine based on the body's needs. This process involves filtering waste products from the blood and adjusting the composition of the urine accordingly.

The kidneys play a crucial role in maintaining the body's fluid balance. They regulate the volume of extracellular fluid (ECF) and maintain the precise concentration of electrolytes (like sodium, potassium, and calcium) in the blood.

The kidneys maintain the appropriate pH balance in the blood. They regulate the excretion of hydrogen ions (H+) and bicarbonate ions (HCO3-), which are essential for acid-base equilibrium.

The kidneys remove waste products and harmful substances (toxins and metabolites) from the bloodstream, preventing their accumulation in the body.

Renin, an enzyme produced by the kidneys, plays a key role in regulating blood pressure by initiating the renin-angiotensin-aldosterone system (RAAS).

Erythropoietin, a hormone secreted by the kidneys, stimulates the production of red blood cells in the bone marrow. This helps maintain adequate oxygen levels in the blood.

The kidneys activate vitamin D3, a crucial vitamin for calcium absorption in the gut. This process aids in maintaining bone health.

Renal blood flow (RBF) is the volume of blood delivered to the kidneys per minute, representing a significant proportion of the body's total blood output.

Autoregulation ensures that RBF remains relatively constant within a specific pressure range, despite variations in blood pressure, maintaining efficient glomerular filtration.

Aldosterone, a hormone produced by the adrenal glands, promotes sodium reabsorption and potassium excretion in the distal tubules, thus influencing fluid balance and blood pressure.

Diuretics are medications that are widely prescribed to enhance the excretion of water and sodium (Na+) in urine, leading to a decrease in plasma volume and blood pressure.

Diuretics are used to manage various conditions, including hypertension (HTN), congestive heart failure (CHF), kidney and liver diseases, as well as intracranial and intraocular pressure.

Carbonic anhydrase inhibitors, like acetazolamide, block the enzyme carbonic anhydrase, primarily in the proximal convoluted tubule (PCT) and also in the collecting duct (CD), leading to reduced reabsorption of sodium (Na+), bicarbonate (HCO3-), and water.

Acetazolamide, a carbonic anhydrase inhibitor, primarily serves as a weak diuretic for reducing intraocular pressure. Its effects include increased sodium (Na+), bicarbonate (HCO3-), and water excretion, rendering the urine alkaline.

Acetazolamide can cause metabolic acidosis due to its effect on bicarbonate (HCO3-) reabsorption. Other side effects include hypokalemia, hyperchloremia, kidney stones, fatigue, and paresthesias.

Osmotic diuretics, such as mannitol, urea, isosorbide, and glycerin, are filtered freely by the glomerulus and increase the osmolarity of fluids. They primarily work in the proximal convoluted tubule (PCT) and the descending limb of the Loop of Henle.

Osmotic diuretics have various therapeutic applications, including preventing perioperative renal failure by dilating blood vessels, improving renal blood flow, and removing toxins and debris. They also act as scavengers of free oxygen radicals.

Osmotic diuretics can lead to side effects such as dehydration (hypovolemia), particularly with long-term use. Other side effects include hypokalemia, hyponatremia, and thrombophlebitis.

Mannitol, a sugar alcohol, is a commonly used osmotic diuretic. It is administered intravenously (IV) with an onset of action between 10-15 minutes.

Thiazides primarily work by blocking the reabsorption of sodium chloride (NaCl) in the distal convoluted tubule of the kidney. This leads to increased excretion of sodium and water, thus promoting diuresis. Unlike loop diuretics, thiazides only act on the distal tubule and don't affect the ascending limb of the loop of Henle.

Acetazolamide mainly disrupts the body's acid-base balance by inhibiting carbonic anhydrase in the proximal convoluted tubule. This enzyme is crucial for bicarbonate reabsorption, so its inhibition leads to increased bicarbonate excretion, causing metabolic acidosis.

Furosemide, a loop diuretic, primarily works by inhibiting the reabsorption of sodium and chloride in the ascending limb of the loop of Henle, increasing urine output.

Spironolactone, an aldosterone antagonist, primarily works on the distal convoluted tubule of the kidney. It blocks the action of aldosterone, a hormone that promotes sodium reabsorption and potassium excretion. This leads to increased potassium retention and sodium excretion, promoting diuresis.

The main side effect of thiazides is hypokalemia (low potassium levels). Thiazides promote potassium excretion, leading to potential imbalances.

Acetazolamide, a carbonic anhydrase inhibitor, can cause metabolic acidosis, hypokalemia (low potassium levels), and hyperchloremia (high chloride levels).

Furosemide can cause ototoxicity (damage to the auditory system), especially in patients with impaired renal function or those receiving high doses.

Both furosemide (a loop diuretic) and ethacrynic acid can cause ototoxicity, particularly in individuals with renal impairment or receiving high doses.

A class of diuretics that block the sodium-chloride cotransporter in the distal convoluted tubule, leading to reduced reabsorption of sodium, chloride, and water, increased potassium excretion, and increased calcium reabsorption.

The primary use of thiazide diuretics is as first-line treatment for hypertension. They can also be used to manage edema (swelling) from various conditions like cardiac, renal, or liver failure. Additionally, they can be beneficial in treating hypocalcemia and calcium-containing renal stones.

Common side effects of thiazide diuretics include hypokalemia (low potassium), hyponatremia (low sodium), hypercalcemia (high calcium), hypochloremia (low chloride), hypomagnesemia (low magnesium), hypophosphatemia (low phosphate), and hyperuricemia (high uric acid).

Thiazide diuretics can cause metabolic disturbances like hypovolemia (low blood volume), orthostatic hypotension (low blood pressure when standing), and glucose intolerance with insulin resistance.

The primary action of potassium-sparing diuretics is to promote potassium retention in the body, primarily in the cortical collecting duct of the kidney. They also have some effect on the distal convoluted tubule.

Two main mechanisms characterize Potassium-sparing diuretics: 1. Epithelial Sodium Channel (ENaC) Blockers: These medications prevent sodium and water reabsorption by blocking the ENaC in the collecting duct. Examples include triamterene and amiloride. 2. Aldosterone Receptor Antagonists: These medications block the action of aldosterone, a hormone that promotes sodium retention and potassium excretion. This reduces sodium and water reabsorption, inhibits the sodium-potassium ATPase, and ultimately leads to increased potassium retention. Examples include spironolactone and eplerenone.

Common side effects associated with potassium-sparing diuretics include hyperkalemia (high potassium), hyponatremia (low sodium), metabolic acidosis, dehydration, orthostatic hypotension, gynecomastia (breast enlargement in men), decreased androgen levels (male hormones), and dry skin or rashes.

These agents work by activating dopamine D1 receptors. This leads to increased cAMP levels, inhibition of Na+/H+ exchange, inhibition of Na+/K+ ATPase, increased sodium excretion (natriuresis), and maintenance or improvement of renal blood flow (RBF) and glomerular filtration rate (GFR).

At higher doses, dopamine receptor agonists can stimulate the sympathetic nervous system, leading to beta cardiac stimulation (increased heart rate and contractility) and alpha vasoconstriction (narrowing of blood vessels).

Fenoldopam is a selective D1 receptor agonist with modest activity at alpha-2 receptors. It has no known effect on D2, beta, or alpha-1 receptors. Its benefits include increased renal blood flow and reduced systemic vascular resistance. It is used for short-term treatment of severe hypertension and renal protection in high-risk patients. Its fast-acting nature, with a half-life of 10 minutes, makes it effective for quickly lowering blood pressure.

Diuretics are medications that increase urine production by promoting the excretion of water and electrolytes. Different classes of diuretics act at various sites in the nephron, the functional unit of the kidney, to achieve their effects.

Loop diuretics are potent diuretics that work in the ascending loop of Henle of the nephron. They block the sodium-potassium-chloride cotransporter, leading to reduced reabsorption of sodium, potassium, and chloride, and an increase in urine output.

Loop diuretics can cause a variety of side effects, including hypokalemia (low potassium), hyponatremia (low sodium), hypomagnesemia (low magnesium), ototoxicity (damage to the ear), and hyperuricemia (high uric acid).

Loop diuretics are often used as a first-line treatment for heart failure, edema (swelling), and hypertension, particularly in patients with renal impairment.

A specific type of loop diuretic, furosemide, is used to treat certain types of acute kidney injury (AKI) and is also beneficial in the treatment of acute hypercalcemia (high calcium) to promote urinary calcium excretion.