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Flashcards in Renal Deck (76)
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Pronephros, mesonephros, and metanephros

Pronephros: Present at week 4; later degenerates

Mesonephros: interim kidney for first trimester; later contributes to male genital system

Metanephros: appears in 5th wk gestation, forms permanent kidney. ureteric bud form mesonephric duct gives rise to ureter, pelvises, calyces, collecting ducts. metanephric mesenchyme gives rise to glomerulus through distal convoluted tubule


Potter sequence

Oligohydramnios causes compression of developing fetus leading to limb deformities and facial anomalies, compression of chest, lack of aspiration of fluid into fetal lungs leading to pulmonary hypoplasia

Causes: ARPKD, obstructive uropathy, bilateral renal agenesis


Horseshoe kidney

Inferior poles of kidneys fuse; gets trapped under inf mesenteric artery as kidneys ascend


Multicystic dysplastic kidney

Caused by abnormal interaction between ureteric bud and metanephric mesenchyme. Nonfunctional kidney of cysts and connective tissue


Duplex collecting system

bifurcation of ureteric bud creating bifid ureter; associated iwth vesicoureteral feflux, ureteral obstruction, UTIs


Path of ureters

Under uterine artery and under ductus deferens (water under the bridge)


Fluid breadkwon of body

60% of body made of water
40% ICF; 20% ECF


Glomerular giltration barrier

Filters plasma by size and charge. Consists of fenestrated endothelium, fused BM containing heparan sulfate (neg charge barrer), epithelial layer with podocyte foot processes


Formula for renal clearance

C=UV/P=volume of plasma from which substance completely cleared per unit time

U=urine concentration of X
P=plasma concentration of X
V=urine flow rate


Formula for GFR

GRF = clearance of inulin = Uinulin x V/Pinulin
works because inulin neither reabsorbed nor secreted


Filtration fraction

fraction of circulating plasma that gets filtered into the tubules

normal is 20%


Hartnup disease

AR deficiency of neutral amino acid transporters in proximal renal tubular cells and on enterocytes resulting in neutral aminoa cids in urine and decreased absorption from the gut

Results in pellagra like symptoms due to decreased tryptophan converstion to niacin


Function of early PCT

-reabsorbs all glucose and amino acids
-reabsorbs most ions isotonically
-generates and secretes NH3 to buffer secreted H+
-responds to PTH to decreased phosphate reabsorption
-responds to AT II to increase Na+ reabsortipon via Na+/H+ exchange (permits contraction alkalosis)


Function of loop of henle

Thin descending loop:
-passively reabsorbs H2O via medullary hypertonicity
-concentrates urine

Thick ascending loop
-reabsorbs Na+, K+, Cl-
-paracellular reabsorption of Mg++ and Ca++
-impermeable to water - makes urine less concentrated


Function of early DCT

-reabsorbs Na+ and Cl- making urine dilute
-increases Ca++ reabsorption in response to PTH


Function of collecting tubule

-reabsorbs Na+ in exchange for secretion of K+ and H+ (aldo regulated)
-reabsorbs more water in response to ADH


Aldosterone actions

All in collecting tubule
-principles cells: increases apical K+ conductance, increases Na+/K+ pump, increases ENaC channels
-intercalated cells: increases H+ ATPase activity which increases the HCO3-/Cl- exchanger


Fanconi syndrome

Reabsorptive defect in PCT. Increased excretion of amino acids, glucose, bicarb, and phosphate. Can cause metabolic acidosis.

Can be caused by ischemia, multiple myeloma, nephrotoxic drugs, lead poisoning


Bartter syndrome

Reabsorptive defect in thick ascending loop due to effect in Na+/K+/2Cl- co transporter. AR. Hypokalemia and metabolic alkalosis, hypercalciuria.


Gitelman syndrome

Reabsorptive defect of NaCl in DCT. AR. Hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria.


Liddle syndrome

AD gain of funtion mtation that increases Na+ reabsorption in collecting tubules


Syndrome of apparent mineralocorticoid excess

Deficiency of 11beta hydroxysteroid dehydrogenase: excess cortisol increases mineralocorticoid receptor activity leading to HTN, hypokalemia, metabolic alkalosis. Can acquire from licorice which blocks this enzyme.


Actions of angiotensin II (five)

-constricts efferent arteriole to increase filtration fraction and GFR despite low volume
-promotes aldosterone and ADH secretion
-increases Na+/H+ exchange in proximal collecting tubule
-stimulates hypothalamus leading to thirst


Stimuli for angiotensin II release (3)

Decreased BP sensed by JG cells
Decreased distal delivery of Na+ to macula densa cells
Increased sympathetic tone via beta1 receptors

All stimulate renin which leads to activation of angiotensinogen to angiotensin I


Activity of ANP and BNP

Released from atria and ventricles in response to increased volume. Relax vascular smooth muscle to increase GFR and decrease renin (check on RAAS system)


JG apparatus

Consists of mesangial cells, JG cells (modifed afferent arteriole smooth muscle), macula densa (NaCl sensor that is part of DCT)

Secretes renin in response to decreased renal BP and increased sympathetic tone


Prostaglandins in the kidney

Vasodilate afferent arteriole to increase RBF. Block by NSAIDs leads to constriction of afferent and decreased GFR


Things that shift K+ out of cells (six)

Do LABS: digitalis, hyperosmolarity, lysis of cells, acidosis, beta blocker, high blood sugar


things that shift K+ into cells (four)

Beta agonists


Presentation of hypo and hyperkalemia

Hypo: U waves, flattened waves, arrhythmia, muscle spasm

Hyper: Wide QRS, peaked T waves, arrhythmias, muscle weakness