15(kidneys) Flashcards
(20 cards)
What is the typical normal GFR in a young healthy adult, and how does it change with age?
Normal GFR is about 120–125 mL/min. GFR declines gradually with age (e.g., by 1 mL/min per year after age 40), so elderly individuals often have lower ‘normal’ GFR.
How do clinicians classify stages of chronic kidney disease (CKD) based on estimated GFR?
CKD stages are defined as: Stage 1 (GFR ≥90 with kidney damage), Stage 2 (60–89), Stage 3a (45–59), Stage 3b (30–44), Stage 4 (15–29), Stage 5 (<15, kidney failure).
What major functions, beyond filtration, do the kidneys perform to maintain homeostasis?
Control of blood composition (fluid/electrolyte balance), regulation of blood volume and pressure, endocrine functions (erythropoietin and calcitriol production), acid-base balance, and excretion of metabolic wastes (urea, uric acid, creatinine).
How do the kidneys contribute to acid-base balance through bicarbonate reabsorption?
In proximal tubule cells, filtered HCO₃⁻ combines with secreted H⁺ to form CO₂ + H₂O (via carbonic anhydrase). CO₂ diffuses into cells, is reconverted to HCO₃⁻, which is reabsorbed with Na⁺, while H⁺ is secreted back into lumen.
What role does renal ammoniagenesis (glutamine metabolism) play in acid excretion?
Glutamine is metabolized in proximal tubule cells to produce NH₄⁺ and HCO₃⁻. NH₄⁺ is secreted into filtrate (excreting acid), while HCO₃⁻ enters peritubular capillaries (replenishing blood buffer).
How can the kidneys compensate for metabolic acidosis?
By increasing H⁺ secretion and NH₄⁺ excretion, reabsorbing more HCO₃⁻, and generating new HCO₃⁻ via glutamine metabolism, thus restoring blood pH toward normal.
What is the countercurrent exchange mechanism in the vasa recta?
Blood in the vasa recta flows opposite to filtrate in the loop of Henle. As blood descends into the medulla, it picks up solutes and loses water; as it ascends, it loses solutes and gains water. This preserves the medullary osmotic gradient.
How do the kidneys regulate blood pressure through the renin–angiotensin–aldosterone system (RAAS)?
Juxtaglomerular cells release renin in response to low renal perfusion. Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II (a vasoconstrictor) by ACE. Angiotensin II stimulates aldosterone release, increasing Na⁺/water reabsorption and raising blood pressure.
What stimuli trigger renin release from juxtaglomerular cells?
Decreased stretch of afferent arteriole (low renal perfusion pressure), reduced NaCl delivery to macula densa, and sympathetic β₁-adrenergic stimulation.
Through which mechanism does angiotensin II directly increase GFR in early hypovolemia?
At low to moderate levels, angiotensin II preferentially constricts efferent arterioles (more than afferent), increasing glomerular capillary pressure and helping maintain GFR despite reduced renal perfusion.
What hormones do the kidneys produce that affect erythropoiesis and calcium homeostasis?
Erythropoietin (EPO) from peritubular interstitial cells stimulates red blood cell production in bone marrow. Calcitriol (active vitamin D) produced by 1α-hydroxylase in proximal tubule cells enhances intestinal Ca²⁺ absorption.
How does decreased renal function lead to anemia?
Impaired kidneys produce less erythropoietin, resulting in reduced stimulation of erythrocyte production, causing anemia in chronic kidney disease.
In the proximal tubule, what transporter exchanges Na⁺ for H⁺, and why is this important?
The Na⁺/H⁺ exchanger (NHE) secretes H⁺ into filtrate in exchange for Na⁺ reabsorption. This process is vital for reclaiming filtered bicarbonate and regulating acid-base balance.
Describe how loop diuretics affect the countercurrent multiplier and medullary gradient.
Loop diuretics (e.g., furosemide) inhibit Na⁺-K⁺-2Cl⁻ cotransporters in the thick ascending limb, preventing ion reabsorption that normally dilutes the ascending limb. This disrupts the medullary gradient, reducing water reabsorption in the collecting duct and causing diuresis.
What is the significance of the filtration coefficient (Kf) in GFR?
Kf reflects the total surface area and permeability of glomerular capillaries. Changes in Kf (e.g., due to glomerular damage reducing surface area) directly decrease GFR.
How do prostaglandins influence GFR and renal blood flow?
Prostaglandins (e.g., PGE₂, PGI₂) dilate afferent arterioles, increasing renal blood flow and GFR. They counteract excessive vasoconstriction from sympathetic stimulation or angiotensin II.
Why might NSAIDs impair renal function in susceptible individuals?
NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis. Without prostaglandin-mediated afferent arteriole dilation, GFR may drop, especially under conditions dependent on prostaglandins (e.g., dehydration, heart failure).
What laboratory values change in acute kidney injury regarding BUN and creatinine?
In acute kidney injury, both blood urea nitrogen (BUN) and serum creatinine rise due to reduced GFR. The BUN:creatinine ratio may help distinguish pre-renal (ratio >20:1) from intrinsic renal (ratio ~10–15:1) causes.
How does the kidney participate in potassium homeostasis?
The distal tubule and collecting duct secrete K⁺ via principal cells under the influence of aldosterone (increases Na⁺ reabsorption and K⁺ secretion). This maintains plasma K⁺ within a narrow range.
What is the renal handling of glucose under normal conditions, and what happens in uncontrolled diabetes mellitus?
Normally, nearly all filtered glucose is reabsorbed in the proximal tubule via sodium–glucose cotransporters. In diabetes, plasma glucose may exceed the transport maximum (Tm) of these transporters, resulting in glycosuria.
