1
What are the steps of urine formation
Filtration - Bulk movement of fluid
Resorption - filtrate to capillaries
Secretion - capillaries to filtrate
Excretion - out of the body
What communication exists between the DCT and the afferent arteriole
Paracrine from the macula densa in response to Na+ conc.
What type of capillaries makes up the glomerular tuft
Fenestrated
What is (volume) normal urine output
>0.5ml/kg/day
Define (volume) oliguria and anuria
Oliguria <400ml/day
Anuria <100ml/day
What are the three primary functions of the kidney?
Excretion of waste
Water and ion homeostasis
Endocrine signaling
List and describe the starlings forces acting at the glomerulus
Capillary hydrostatic
Bowmen capsular oncotic
Bowmen Capsular hydrostatic
How do starlings forces (Bowmen capsular only) change across the glomerular capillary bed
Oncotic increases as fluid is filtered out concentrating plasma proteins
Hydrostatic is unchanged
What are the main classifications of renal failure - one example of each
Pre-renal - Hypovolemia (dehydration, sepsis, burns ect.)
Intrarenal/intrinsic - glomerulonephritis, ATN, DM
Post-renal - BPH, calculi, tumor
What region of the nephron is most water reabsorbed
PCT
What are the components of the juxtaglomerular aparatus?
JG cells
Macula densa cells
Extraglomerular mesangial cells
How do NSAIDs and ACEI affect GFR
ACEI - ACEI cause efferent arteriole dilation
Add in a diuretic and this is the 'triple whammy' of renal death
Quick, medium, long term mechanisms for correcting acid-base disruptions
Quick - buffer systems
Medium - respiratory
long - renal
How is the interstitial concentration gradient which drives fluid reabsorption created
Countercurrent multiplication
Uses ATP to build up the concentration gradient in the intersitium by reabsorbing solutes in ascending limb LOH
What are the two main factors that stimulate the release of ADH (comment on their sensitivity)
Extracellular fluid osmolarity (highly sensitive~1% change from baseline needed)
Blood pressure (less sensitive ~ 10% change from baseline needed)
What factors affect GFR
Intrinsic - Tubuloglomerular feedback, myogenic response
Extrinsic - SNS, RAAS
What are the triggers for renin release
Afferent arteriolar stretch mechanism
SNS
Macula densa paracrine (reduced GFR = reduced renal Na+ in DCT - increased paracrine signal)
pH: 7.30
HCO3-: 30
Co2: 50
Respiratory acidosis with partial metabolic compensation/alkalosis
pH: 7.47
HCO₃⁻: 36 mmol/L
CO₂: 50 mmHg
Metabolic alkalosis with partial respiratory compensation
Explain countercurrent multiplication
In the thick ascending LOH - Sodium transporters move Na+ into the medulla resulting in increased concentration in the medulla, and a gradient with the tubule.
This part of the LOH is impermeable to water but the thin descending LOH allows water out.
List 4 signs of fluid overload
Peripheral/sacral pitting oedema
Pulmonary oedema
JVD
Rapid Weight gain
HTN
How does the presence or absence of antidiuretic hormone (ADH) affect urine volume and osmolarity?
With ADH: distal nephron becomes permeable to water, water reabsorbed into medulla, low-volume, high-osmolarity urine.
Without ADH: collecting duct impermeable to water, no reabsorption despite medullary gradient, high-volume, low-osmolarity urine.
How do the descending and thick ascending limbs of the Loop of Henle differ in permeability, and what is the main function of this difference?
Descending limb: permeable to water, impermeable to solutes.
Thick ascending limb: impermeable to water, actively reabsorbs Na⁺, K⁺, and Cl⁻.
They establish the medullary osmotic gradient, critical for urine concentration
What are the two main hormones which regulate transport in the distal nephron, and what specific ions or solutes do they affect?
ADH (vasopressin): increases water reabsorption.
Aldosterone: increases Na⁺ reabsorption and K⁺ secretion.
What is meant by the transport maximum
Transport maximum is the point at which all membrane carriers for a substance are saturated. Once plasma concentration exceeds this, reabsorption cannot keep up with filtration, and the excess solute begins to appear in urine (I.E., glucose)