Kidney 2

Sodium enters passively down the [blank_start]apical[blank_end] membrane down its concentration gradient. It is actively extruded across the basolateral membrane by the Na/K/ATPase pump. Na+ reabsorption is [blank_start]largest[blank_end] in the PCT, followed by the LOH, DCT and CD. In the PCT- [blank_start]Na/H[blank_end] exchanger at the apical membrane, at the basolateral membrane NA/K/ATPase and Na/HCO3 transporter. In the thick limb of the LOH [blank_start]Na/K/Cl[blank_end]- cotransporter (NKCC2)...which can be inhibited by [blank_start]frusemide[blank_end], 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. [blank_start]Water[blank_end] reabsorption in the proximal tubule is linked to Na+ reabsorption.

[blank_start]Angiotensin 2[blank_end] 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 [blank_start]sodium[blank_end] 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 [blank_start]high[blank_end] 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 [blank_start]PCT[blank_end] as well. The [blank_start]principle[blank_end] cell is the Major Regulator of Potassium with [blank_start]90[blank_end]% of potassium being managed here. The Epithelial Na Channels gets us to dump all the potassium by an [blank_start]electrochemical[blank_end] gradient The [blank_start]more[blank_end] 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 [blank_start]Na/K/Cl[blank_end]- contransporter. In the cortical collecting duct- K+ reabsorption by intercalated discs occurs through the apical K+ uptake mediated by the [blank_start]H-K[blank_end] Pump, followed by passively efflux across the basolateral membrane. In the cortical collecting ducts (principle cells), the K+ [blank_start]secretion[blank_end] occurs by active uptake across basolateral membrane, followed by passive diffusion through apical K+ channels.

Stimulators of K+ excretion include?

Chloride is reabsorbed via the [blank_start]paracellular[blank_end] 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 [blank_start]Na[blank_end]+ out of lumen. At the basolateral membrane via Cl- channels and K/Cl- cotransporter. In the thick ascending limb via [blank_start]Na/K/2Cl[blank_end]- cotransporter. In the [blank_start]collecting[blank_end] ducts via paracellular reabsorption, apically via Cl-HCO3- exchanger and Cl- channels basolateral membrane.

What are the two most important regulators of calcium?

Most (80%) of the phosphate is reabsorbed at the PCT. Which factors increase phosphate reabsorption?

The pre-renal causes of AKI include?

Renal causes of AKI include?

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?

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 <[blank_start]0.5mL[blank_end]/kg per hour for 6 hours I- ([blank_start]Injury[blank_end]) = 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 [blank_start]anuria[blank_end] 12 hours L- (Loss) = complete loss of kidney function > [blank_start]4 weeks[blank_end] 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?

The classic triad of Acute Interstitial Nephritis is: [blank_start]Fever[blank_end], Eosinophilia and [blank_start]Rash[blank_end]. It is most commonly caused by drugs such as [blank_start]flucloxacillin[blank_end], [blank_start]rifampin[blank_end] and NSAID's. It often [blank_start]resolves spontaneously[blank_end] after halting these.

Hyperkalemia is a common problem of AKI. The mainstay of treatments are -[blank_start]B2 agonist[blank_end] to drive K+ intracellularly -Resonium which exchanges K+ and Na+ in the large intestine reducing intake -Insulin and Glucose which drives K+ intracellularly -[blank_start]Calcium gluconate[blank_end] to correct myocardium potential

Which of these is not a role of the mesangium (the space between the capillaries of glomerulus)?

A thin layer of [blank_start]fenestrated[blank_end] endothelial cells with tight junctions surround the capillary lumen

Nephrotic Syndrome is characterised by:

NSAID's, ACE-Inhibitors and Diuretics can impair kidney function by?