Sodium enters passively down the membrane down its concentration gradient. It is actively extruded across the basolateral membrane by the Na/K/ATPase pump. Na+ reabsorption is in the PCT, followed by the LOH, DCT and CD.
In the PCT- exchanger at the apical membrane, at the basolateral membrane NA/K/ATPase and Na/HCO3 transporter.
In the thick limb of the LOH - cotransporter (NKCC2)...which can be inhibited by , leading to increased sodium in the DCT and therefore less water loss.
Na transport in the DCT is via transcellular reabsorption (Na/Cl transporter NCC)--thiazide diuretics can inhibit this.
In the cortical collecting duct, Na transport is mediated primarily by the principle cells. It crosses through ENAC's and can be inhibited by amiloride. reabsorption in the proximal tubule is linked to Na+ reabsorption.
Angiontensin 1( Angiotensin 2, Angiontensin 1 ) binds to AT1 receptors of the proximal tubule. They also stimulate Na-H exchange in the TAL and ENAC's in the initial collecting tubules. All promote sodium
potassium( sodium, calcium, potassium ) reabsorption.
Aldosterone stimulates sodium reabsorption by the initial tubule and CCT. It upregulates apical ENAC's and therefore Na+ permeability.
ADH- overall effect is to produce urine which a high
low( high, low ) osmolality. In the TAL, ADH stimulates NKCC2 receptors and K+ channels. In the principle cells of the initial collecting tubule and CCT, ADH stimulates Na+ transport by increasing the number of open Na+ channels.
Most of the K is absorbed in the as well. The cell is the Major Regulator of Potassium with % of potassium being managed here.
The Epithelial Na Channels gets us to dump all the potassium by an gradient
The sodium delivered the more potassium dumped. In the proximal tubule K+ reabsorption occurs passively and is via solvent drag. In the TAL K+ is reabsorbed paracellularly and through the - contransporter. In the cortical collecting duct- K+ reabsorption by intercalated discs occurs through the apical K+ uptake mediated by the Pump, followed by passively efflux across the basolateral membrane. In the cortical collecting ducts (principle cells), the K+ occurs by active uptake across basolateral membrane, followed by passive diffusion through apical K+ channels.
Stimulators of K+ excretion include?
Increased K+ intake
Increased sodium delivery
Chloride is reabsorbed via the pathway early in the PCT via solvent drag,
Later in the PCT at the apical memrane via Cl-base exchanger (Cl- out of lumen, Base in), following + out of lumen. At the basolateral membrane via Cl- channels and K/Cl- cotransporter.
In the thick ascending limb via - cotransporter.
In the ducts via paracellular reabsorption, apically via Cl-HCO3- exchanger and Cl- channels basolateral membrane.
What are the two most important regulators of calcium?
Na and PTH
PTH and Vitamin D
TSH and Vitamin D
PTH and K
Most (80%) of the phosphate is reabsorbed at the PCT.
Which factors increase phosphate reabsorption?
high plasma calcium
low plasma calcium
The pre-renal causes of AKI include?
Renal causes of AKI include?
Acute tubular necrosis
Acute Interstitial Nephritis
A serum creatinine level of 2-3 x the normal amount would place the person in which stage of kidney disease?
Which of these is not a novel biomarker for acute kidney injury?
Urinary Neutrophil Gelatinase- Associated Lipocalin
Urinary Kidney-Injury molecule 1
In the RIFLE classification of AKI. Describe the following components.
R- (Risk) = 1.5 x increase in serum creatinine, GFR less 25% or urine output <0.5mL
1mL( 0.5mL, 1mL )/kg per hour for 6 hours
Ischaemia( Injury, Ischaemia )) = 2 x serum creatinine, GFR 50%, or urine output <0.5mL/kg for 12 hours
F- (Failure) = 3 x SC, GFR 75% drop, urine output <0.5mL/kg 24 hours or anuria
proteinuria( anuria, proteinuria ) 12 hours
L- (Loss) = complete loss of kidney function > 4 weeks
12 weeks( 4 weeks, 8 weeks, 12 weeks )
E- (ESRD) = > 3 months
Acute Tubular Necrosis is due to tubular injury and prolonged disturbances in blood flow. Which of these is not a common histological feature?
Loss of brush border
Distal tubule casts
Areas of cellular regeneration
Low tubule calcium
The classic triad of Acute Interstitial Nephritis is: , Eosinophilia and .
It is most commonly caused by drugs such as , and NSAID's.
It often after halting these.
Hyperkalemia is a common problem of AKI. The mainstay of treatments are
- to drive K+ intracellularly
-Resonium which exchanges K+ and Na+ in the large intestine reducing intake
-Insulin and Glucose which drives K+ intracellularly
- to correct myocardium potential
Which of these is not a role of the mesangium (the space between the capillaries of glomerulus)?
Provide structural support to glomerulus
Proliferation and laying down of collagen
A thin layer of endothelial cells with tight junctions surround the capillary lumen
Nephrotic Syndrome is characterised by:
Large amount of Red Blood Cells
Heavy protein > 3.5g/ day
NSAID's, ACE-Inhibitors and Diuretics can impair kidney function by?
Dilation of afferent arteriole
Constriction of afferent arteriole
Dilation of efferent arteriole
Constriction of efferent arteriole
Promoting increased perfusion via volume expansion
Promoting decreased perfusion via volume contraction