Pronephros
week 4 then degenerates
Mesonephros
functions as interim kidney for 1st trimester; later contributes to male genital system
metanephros
permanent, first appears in 5th week of gestation; nephrogenesis continues though 32-36 weeks of gestation
ureteric bud
derived from the caudal end of the mesonephric duct; gives rise to the ureter, pelvices, calyces and collecting ducts, fully canalized by the 10th week
The kidneys are derivitives of?
mesoderm
the urethra is a derivitive of?
endoderm
Metanephric mesenchyme and utereric bud interact
the interaction induces differentiation and formation of glomerulus through to distal convoluted tubule, if the interaction goes wrong –> congenital malformations
Ureteropelvic junction
last to canalize –> most common site of obstruction (hydronephrosis) in fetus
Potter sequence
oligohydramnios –> compression of developing fetus –> limb deformities, facial anomalies (low sets ears and retrognathia), compression of chest (pulmonary hyperplasia leads to death)
causes include: ARPKD, posterior urethral valves and bilateral renal angenesis
Potter mnemonic
Pulmonary hypoplasia oligohydramnios twisted face twisted skin extremity defects renal failure in utero
horse shoe kidney
- inferior poles of both kidneys fuse
- as the ascend from pelvis during fetal development they get trapped under the IMA and remain low in the abdomen.
- kidney function is normal
- increased risk for ureteropelvic junction obstruction, hydronephrosis, renal stones and rarely renal cancer (wilms tumor)
assoc with TURNERS
multicystic dysplastic kidney
-due to abnormal interaction of the ureteruc bud and the metanephric mesenchyme —> cysts and connective tissue issues and non functioning kindey, can be seen on US
What do we use to estimate the GFR? why?
Creatinine
GFR = clearance of creatinine = UV/P
it is freely filtered, not reasorbed and not secreted, well just a tiny bit of secretion
What do we use to measure RPF?
PAH, to measure the ERPF = UV/P = clearance of PAH
RBF= RPF (1-hct)
PAH is both filtered and actively secreted in the proximal tubule, nearly all PAH entering the kidney is excreted
Hartnup disease
autosomal recessive disorder
- deficiency of neutral amino acid transporters in the PT.
- lose tryptophan, need tryptophan to make niacin with the help of B6
- pellagra (diarrhea, dementia and dermatitis)
Fanconi syndrome
- reabsorption defect in PT
- assoc with increase excretion of nearly all amino acids, glucose, HCO3 and PO4
- may result in metabolic acidosis
- type II renal acidosis (cant reabsorm HCO3/make)
Bartter sydrome
- reabsorption defect in thick ascending loop
- Na/K/2Cl transporter, autosomal recessive
- lead to hypokalemia and metabolic alkalosis with hypercalciura (Mg and Ca will not be reabsorbed)
Gitelman syndrome
- autosomal recessive
- DCT
- Na/Cl channel defect
- like a thiazide so more calcium resorbed
- hypokalemia and metabolic alkalosis
Liddle syndrome
Autosomal dominant
- increased Na reabsorption in distal and collecting tubules (increased activity of the Na channel)
- result in HTN
- hypokalemia
- metabolic alkalosis
- decrease aldosterone
treat: amiloride
Where is EPO made?
interstitial cells in the peritubular capillary bends
Where does vitamin D get activated?
Proximal tubule
What affect does prostaglandins have on the kidney?
paracrene sections vasodilate the AFFERENT arterioles leading to increase RBF.
-so if we have NSAIDS this will block the renal protective prostaglandin and lead to decreased GFR which may result in renal failure
Anion gap metabolic acidosis
MUDPILES
methanol uremia diabetic ketoacidosis propylene glycol iron tablets or INH lactic acidosis ethylene gylcol salicylate toxicity late
normal anion gap metabolic acidosis
HARD-ASS
Hyperalimentation addison disease renal tubular acidosis diarrhea acetazolamide spirinolactone saline infusion
