Renal- Physiology Flashcards
Renal clearance
Cx = (UxV)/Px = volume of plasma from which the substance is completely cleared per unit time.
Effective renal plasma flow (eRPF)
estimated using para-aminohippuric acid (PAH) clearance.
eRPF = UPAH× V/PPAH = CPAH.
Renal blood flow (RBF) = RPF/(1 − Hct).
Plasma volume = TBV × (1 – Hct).
Filtration
Filtration fraction (FF) = GFR/RPF. Normal FF = 20%. Filtered load (mg/min) = GFR (mL/min) × plasma concentration (mg/mL).
Changes in glomerular dynamics
- increase in plasma protein concentration
- Decrease in plasma protein concentration
Decrease GFR
Increase GFR
Calculation of reabsorption and secretion rate
Filtered load = GFR × Px.
Excretion rate = V × Ux.
Reabsorption rate = filtered – excreted.
Secretion rate = excreted – filtered.
Splay phenomenon
Tm for glucose is reached gradually rather than sharply due to the heterogeneity of nephrons
Glucose clearance
Plasma glucose of ∼ 200 mg/dL, glucosuria begins (threshold). At rate of ∼ 375 mg/min, all transporters are fully saturated (Tm).
Fanconi syndrome
- Deffect
- Effect
- Etiology
Defect in PCT excretion of amino acids, glucose,
HCO3, and PO4, and all substances reabsorbed by the
PCT
Proximal RTA, hypophosphatemia, osteopenia
Hereditary defects, ischemia, multiple myeloma,
nephrotoxins/drugs, lead poisoning
Bartter syndrome
- Deffect
- Effect
Defect in thick ascending loop of Henle. AR
Metabolic alkalosis, hypokalemia, hypercalciuria
Gitelman syndrome
- Deffect
- Effect
Reabsorption defect of NaCl in DCT. AR
Metabolic alkalosis, hypomagnesemia, hypokalemia,
hypocalciuria
Liddle syndrome
- Deffect
- Effect
Gain of function mutation in EnaC. AD
Metabolic alkalosis, hypokalemia, hypertension, decrease aldosterone
Syndrome of Apparent Mineralocorticoid Excess (SAME)
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase. AR
Metabolic alkalosis, hypokalemia, hypertension low aldosterone; cortisol
ANP, BNP
relaxes vascular smooth muscle via cGMP increase GFR, decrease renin.
Dilates afferent arteriole, constricts efferent arteriole, promotes natriuresis.
Juxtaglomerular apparatus
Consists of mesangial cells, JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, located at distal end of loop of Henle)
Kidney endocrine functions
Erythropoietin
Calciferol (vitamin D) (PCT cells)
Prostaglandins (vasodilates afferent artery)
Dopamine (by PCT cells, promotes natriuresis)
- At low doses, dilates interlobular arteries, afferent
arterioles, efferent arterioles
- At higher doses, acts as vasoconstrictor
SHIFTS K+ INTO CELL (CAUSING HYPOKALEMIA)
Hypo-osmolarity
Alkalosis
β-adrenergic agonist
Insulin
SHIFTS K+ OUT OF CELL (CAUSING HYPERKALEMIA)
Digitalis HyperOsmolarity Lysis of cells Acidosis β-blocker} high blood Sugar (insulin deficiency) Succinylcholine
DO LABSS
Electrolyte disturbances clinical manifestations
- Low Na
- High Na
Nausea and malaise, stupor, coma, seizures
Irritability, stupor, coma
Electrolyte disturbances clinical manifestations
- Low K
- High K
U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness
Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
Electrolyte disturbances clinical manifestations
- Low Ca
- High Ca
Tetany, seizures, QT prolongation, twitching
(Chvostek sign), spasm (Trousseau sign)
Stones (renal), bones (pain), groans (abdominal pain), thrones (urinary frequency), psychiatric overtones (anxiety, altered mental status)
Electrolyte disturbances clinical manifestations
- Low Mg
- High Mg
Tetany, torsades de pointes, hypokalemia, hypocalcemia (when [Mg2+] < 1.2 mg/dL)
Increase DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
Electrolyte disturbances clinical manifestations
- Low PO4
- High PO4
Bone loss, osteomalacia (adults), rickets (children)
Renal stones, metastatic calcifications, hypocalcemia
Henderson-Hasselbalch equation
pH = 6.1 + log [HCO3−] / 0.03 PCO2
Normal anion gap Metabolic acidosis
HARDASS: Hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
Increase anion gap Metabolic acidosis
MUDPILES: Methanol (formic acid) Uremia Diabetic ketoacidosis Propylene glycol Iron tablets or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Distal renal tubular acidosis (type 1)
- Defect
- Urine pH and K
- Causes
- Associations
Inability of α-intercalated cells
> 5.5 Urine pH, Decrease K
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune
risk for calcium phosphate kidney stones
Proximal renal tubular acidosis (type 2)
- Defect
- Urine pH and K
- Causes
- Associations
Defect in PCT HCO3– reabsorption excretion of
HCO3 – in urine
< 5.5 pH, decrease K
Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
risk for hypophosphatemic rickets
Hyperkalemic tubular acidosis (type 4)
- Defect
- Urine pH and K
- Causes
Hypoaldosteronism or aldosterone resistance
< 5.5 pH, Increase K
Decrease aldosterone production (eg, diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin,
cyclosporine, adrenal insufficiency)
or
aldosterone resistance (eg, K+-sparing diuretics, nephropathy due to obstruction, TMP-SMX)