Nephrology Pathophysiology Flashcards
What are 5 kidney functions
- Regulate blood volume/pressure
- pH + electrolyte balance
- Stimulation of erythropoiesis
- Supporting vitamin D biosynthesis
- Excretion: elimination of waste products from the body in urine
What is the external anatomy of the kidneys (3 layers)
- Renal fascia (outermost layer): thin, connective tissue that connects kidney to surrounding tissue
- Adipose Capsule (middle layer): fat layer, protects kidney from trauma + maintains positioning
- Renal capsule (innermost layer): connective tissue, maintain kidney shape + protect the inner tissue
What is the internal anatomy of the kidneys?
- Renal cortex: outermost layer
- Renal medulla: middle layer
- Renal pelvis: innermost layer
What are the 3 main stages of excretion in the kidneys
- Glomerular filtration (PASSIVE process): water, SMALL molecules (<5-10kDa)
Unless membrane is damaged, most proteins will NOT pass through here (EN-) - Tubular reabsorption (PASSIVE OR ACTIVE process):
- passive diffusion following conc. gradient
- active transport using membrane-bound enzymes
- Co-transport: Water will follow other molecules that are actively transported (ex. Glucose, sodium ions) - Secretion (ACTIVE process): elimination of LARGE molecules from bloodstream into tubular fluid
What occurs in the 1st step of renal excretion in the renal corpuscle?
- produces renal filtrate
- this is where glomerular filtration (passive) happens
What occurs in the 2nd step of renal excretion in the Proximal convoluted tububle (PCT)? What is unique to its reabsoportion?
primary site of reabsorption
- 80% of filtered bicarbonate is reabsorbed
- Only region that glucose is absorbed in
What occurs in the 3rd of renal excretion in the Loop of Henle LOH?
- Site of urinary concentration
- Differing permeability of ascending and descending limbs create osmotic gradient (facilitates) further reabsorption of water/electrolytes)
What occurs in the 4th step of renal excretion in the Distal convoluted Tubule DCT? What does it play a key role in? (2)
key role in volume + BP regulation
- Contains the Juxtaglomerular apparatus
- Macula densa cells (chemoreceptors): detect changes in solute concentrations
- JG cells (mechanoreceptors): where prorenin -> renin (in drops of BP)
- Extraglomerular mesangial cells
What occurs in the 5th step of renal excretion in the Collecting duct? What hormone is present here?
fine-tuning of filtrate composition
- Most Na + Cl reabsorption is here
- Where aldosterone and anti-diuretic hormone (ADH) act
What is the function of renin?
Released: in response to LOW kidney perfusion pressure OR LOW Na+ concentration (sensed by macula densa cells)
Function: converts angiotensinogen to angiotensin I (then converted to angiotensin II by ACE)
What is the function of angiotensin II?
direct vasoconstriction + stimulation of aldosterone release
What is the function of Aldosterone?
act on collecting duct to retain Na+ and water
What is the final outcome of the RAAS
increased extracellular volume -> increased renal perfusion pressure (once high enough, negative feedback will stop renin release)
What is vasopressin AKA anti-diuretic hormone ADH released in response to? What is its function?
Released: in response to SMALL increase in blood osmolality OR LARGE decrease in intravascular volume
- Released by hypothalamus
Function: increases Na+ concentration in collecting duct -> conserved free water (+ increases active water channels in cell membrane)
- Also stimulates thirst mechanism
Can acute kidney injury happen in CKD?
Yes
What is the criteria for AKI diagnosis?
Any one of these
- Increased SCr by 50% within 7 days
- Increased SCr by 25umol/L within 48 hours
- Oliguria: urine volume <0.5mL/kg/hour for ≥6 hours
What are risk factors for AKI?
Demographics (old age, male, black)
Prior kidney damage (CKD, Diabetes)
Decreased renal perfusion (sepsis, heart failure, volume depletion, major surgery)
Medications (ACEi/ARB, NSAIDs)
How can a patient with AKI present although variable? (5)
- Decreased urine output, urine discolouration
- Edema
- Electrolyte disturbances
- Sudden weight gain
- Severe abdo or flank pain
What physical examination can you take for AKI?
Volume depletion signs:
- postural hypotension
- LOW jugular venous pressure (JVP)
- dry mucous membranes
Fluid overload signs:
- HIGH JVP
- pitting edema
- pulmonary crackles
What lab tests should you order for AKI
SCr vs eGFR/CrCl
Urine output
CBC (to rule out infectious causes)
What is pre-renal AKI a result of?
Decline in rate of GFR proportional to level of hypoperfusion
What are non-drug (3) and drug (2) related causes of pre-renal AKI?
Non-drug
- volume depletion (hemorrhage, diarrhea, skin burns),
- decreased cardiac output (HF, valvular diseases)
- decreased systemic vascular resistance (sepsis)
Drug
- NSAIDs
- RAAS Inhibitors
What is Intrinsic AKI a result of?
- result of damage to renal tubules, glomerulus, vascular structures, interstitium (or from obstruction of renal tubules)
What are non-drug (3) and drug (3) related causes of Intrinsic AKI?
Acute tubular Necrosis
- radiocontrast agents
Acute Interstitial Nephritis
- Antimicrobials (beta-lectams, sulfonamides, quinolones, vanco)
Glomerulonephritis
- Lithium
-NSAIDs
