Renal Disorders

Cortex

outer layer of the kidney

Medulla

inner region of the kidney

Renal Pyramid

triangular structures that contain collecting ducts

Renal Calyx

cup like structures that collect urine from the renal pyramids and drain into the renal pelvis

Renal Pelvis

collects urine from the calyces and channels it into the ureter

Ureter

tube that carries urine from the renal pelvis to the urinary bladder

Renal Artery

supplies oxygenated blood to the kidney for filtration

Renal Vein

drains filtered deoxygenated blood from the kidney into the inferior vena cava

Renal Blood Flow

renal artery = afferent arteriole = glomerulus = efferent arteriole = peritubular capillaries or vasa recta = renal vein

Afferent Arteriole

delivers blood to the glomerulus

vasodilation of arteriole will increase the hydrostatic pressure in glomerulus

this increases GFR

Efferent Arteriole

carry blood away from the glomerulus

vasoconstriction of the arteriole will increase hydrostatic pressure in glomerulus

this also increases GFR

Juxtamedullary Nephrons

long loops of henle extend deep into the medulla

specialized for urine concentration

more susceptible to ischemic injury (due to lower oxygen supply)

Cortical Nephrons

predominately located in the cortex

shorter loops of henle

Nephrons

each kidney has about 1 million of them

you can lose a significant number of them without symptoms

symptoms of CKD often appear when over 50-60% of nephrons are lost

less than 15% remaining nephron function → end stage renal disease treated with dialysis or transplant typically required

Glomerulus

network of capillaries that filters blood

produces protein free cell free filtrate

PCT

reabsorbs 65-70% of filtrate, water, glucose, amimo acids, and electrolytes

secretes acids, drugs, and toxins

Henle Loop

descending limb and water reabsorption

ascending limb reabsorbs Na+, K+, and Cl-

DCT

aldosterone → increases Na+ reabsorption, K+ secretion, and H+ secretion

reabsorbs Ca2+ (stimulated by PTH)

H2O reabsorption

Collecting Ducts

aldosterone → increases Na+ reabsorption, K+ secretion, and H+ secretion

ADH → increases water reabsorption

Ureters

18 inch muscular tubes

use rhythmic contractions (peristalsis) to move urine from the kidneys to the bladder

Urinary Bladder

muscular sac that stores urine

expands contracts to hold and release urine

Urethra

narrow tube that carries urine from the bladder to the outside of the body

Kidney Functions

maintains water, electrolyte, and acid base balance

excretes nitrogenous waste (urea and creatinine)

detoxifies drugs, toxins, and their metabolites

regulates BP and extracellular fluid (ECF) volume with renin angiotensin aldosterone system and ADH

secrete EPO, activate vitamin D, and breakdown hormones

EPO Secretion

kidneys release erythropoietin in response to hypoxia

EPO stimulated the bone marrow to produce more RBCs

Vitamin D Activation

the kidneys convert inactive vitamin D into its active form called calcitriol

calcitriol helps intestines absorb calcium and phosphate

Hormone Breakdown

kidneys help degrade and clear peptide hormones from the blood

this includes insulin, glucagon, and growth hormone

GFR

the rate at which all glomeruli in both kidneys filter blood → 125 mL/min

depends on glomerular capillary hydrostatic pressure (HPgc), glomerular capsular space hydrostatic pressure (HPcs), and glomerular capillary oncotic pressure (OPgc)

Glomerular Capillary Hydrostatic Pressure HPgc

pushes fluid out of capillaries into the capsule

favors filtration

Glomerular Capsular Space Hydrostatic Pressure HPcs

pressure from fluid already in the capsule that resists additional filtration

opposes filtration

Glomerular Capillary Oncotic Pressure OPgc

osmotic pull from plasma proteins that draws water back into capillaries

opposes filtration

Creatinine and GFR

endogenous production → creatinine is continuously produced from skeletal muscle metabolism

freely filtered at glomerulus → passes easily through filtration barrier

not reabsorbed

minimally secreted → small amount secreted into the nephron which means creatinine clearance slightly overestimates true

CrCl

when precise kidney function measurement is needed (extremes of muscle mass, AKI, transplant evaluation)

provides a direct measure of creatinine clearance valves

limitations → requires accurate 24 hour urine collection which is inconvenient and prone to error

Estimated CrCl

used when kidney function is stable and you need it for drug dosing or CKD monitoring

no urine collection required

limitations → doesn’t use urine concentration, less accurate in elderly or malnourished (low muscle mass is low Cr) or muscular ppl (high Cr with normal function)

BUN

measure of the amount of nitrogen in the blood that comes from urea, a waste product formed in the liver from protein metabolism and excreted by the kidneys

ammonia (NH3) is a byproduct of protein metabolism

liver converts ammonia to urea which is less toxic

urea is excreted by the kidneys which is measured as BUN

high → renal failure, dehydration, vigorous exercise

low → liver dysfunction (low urea production) or overhydration

not specific to kidney function, more useful as BUN:creatinine ratio to identify cause of renal dysfunction in acute kidney injury

Complete Blood Count CBC

decreased RBC count due to reduced EPO production by kidneys

decreased Hgb and Hct due to normocytic normochromic anemia

platelet dysfunction from uremia increases bleeding risk despite normal platelet count

Serum Proteins

microalbuminuria → small but abnormal amount of albumin in urea, early sign of glomerular injury

hypoalbuminemia → low albumin in blood seen in later stages due to urinary protein loss

hematuria may occur with glomerular changes

Electrolyte Tests

kidneys lost the ability to reabsorb and secrete them with injury

low bicarb → metabolic acidosis, may see respiratory compensation

hydrogen/potassium shift furthers hyperkalemia

if value is low → loss of reabsorption

if value is high → loss of secretion

low Ca2+ → lack of vitamin D activation

CKD Patho

evidence of kidney damage for 3+ months with or without a decline in GFR or a GFR less than 60 for 3+ months

early stages (over 50% functional nephrons) are often asymptomatic because remaining nephrons compensate

once over 50% of nephrons are lost → compensatory mechanisms fail

waste products accumulate and fluid/electrolyte balance is impaired

non urinary symptoms begin to appear (anemia, bone disease, or fatigue)

CKD Causes

most common causes → hypertension and diabetes mellitus

obstructions like chronic kidney stones

collagen diseases → systemic lupus

nephrotoxic agents → long term aminoglycoside therapy (destroys tubular cells)

Hypertension and CKD

HTN puts too much pressure on glomeruli vessels leading to scarring (glomerulosclerosis) → makes filters leaky and less effective

protein leaks into urine and harms tubules, leading to inflammation and scarring that damages nephrons

reduced kidney perfusion due to arterial narrowing from atherosclerosis (renal artery stenosis)

kidneys try to compensate by releasing renin (makes angiotensin 2) → constricts the efferent arteriole to keep filtering going

this also increases pressure inside the filters and causes even more damage

Diabetes Mellitus and CKD

chronically high glucose damages the glomerular capillaries

this causes basement membrane thickening and glomerular scarring which makes filters less effective

proteins leak into the urine and harm the tubules, which leads to inflammation and scarring

hyperglycemia weakens the immune system increasing the risk of UTIs

pyelonephritis (UTI) especially with poor glucose control

repeated infections cause inflammation and fibrosis leading to progressive nephron damage

CKD Stage 1

GFR of 90 or higher

mild kidney damage but kidneys work as well as normal

CKD Stage 2

GFR of 60-89

mild kidney damage but kidneys still work well

CKD Stage 3a

GFR of 45-59

mild to moderate kidney damage

kidneys don’t work as well as they should

CKD Stage 3b

GFR of 30-44

moderate to severe kidney damage

kidneys don’t work as well as they should

CKD Stage 4

GFR of 15-29

severe kidney damage

kidneys are close to not working at all

CKD Stage 5

GFR less than 15

end stage renal disease

kidneys have failed or are very close to failing

CKD Skin

itching (uremic pruritus) → caused by buildup of urea and phosphate in the skin

pale skin → due to anemia from decreased EPO

easy bruising → platelet dysfunction causing clotting problems

nails → thin, brittle, and may appear spoon shaped due to anemia

hair → becomes dry, scaly, and may fall out easier

CKD GI

anorexia and nausea/vomiting → increased urea suppresses appetite and stimulates chemoreceptor trigger zone

metallic taste and halitosis → urea affects saliva and bacteria in the mouth metabolize it to ammonia which leads to uremic fetor (ammonia breath)

gastric and peptic ulcers → urea irritates stomach lining

GI bleed → platelet dysfunction and mucosal injury from uremia contribute

constipation → results from fluid restriction, phosphate binders (calcium carbonate), and inactivity

CKD Sexual Function

uremia can cause sexual dysfunction

common in both men and women due to hormonal imbalances, anemia, uremia, and psychological stress

men → lower testosterone, erectile dysfunction, and lower libido

women → menstrual irregularities, low fertility, and vaginal dryness

Renal Osteodystrophy

caused by disruption in calcium, phosphate, and vitamin D metabolism in CKD

low kidney function → low calcitriol, low vitamin D activation, low Ca2+ absorption

high phosphate triggers secondary hyperparathyroidism

leads to bone pain, fractures, skeletal deformities, and growth delays in kids

Anemia Treatment

synthetic EPO to stimulate RBC production

blood transfusions if severe

Electrolyte Balance Treatment

calcitriol to increase calcium and lower phosphate

kayexelate or IV insulin + glucose (GIK) → treats hyperkalemia

sodium bicarb to correct metabolic acidosis

BP Treatment

diuretics to manage fluid overload

antihypertensives to control BP and reduce kidney strain

Itching Treatment

antihistamines and corticosteroids

Toxin Removal

dialysis to remove uremic waste products (typically for end stage renal failure)

CKD Diet

low protein → limits urea and other waste buildup

low sodium → helps reduce fluid retention and BP

low potassium → prevents dangerous hyperkalemia

fluid restriction → prevents overload and swelling due to impaired kidney filtration

CKD Diagnosis

ultrasound → shows small atrophic kidneys in advanced CKD

serum labs → high creatinine and BUN and low creatinine clearance, electrolytes will be imbalanced

urine studies → albuminuria and hematuria, low concentrating ability (low SG)

hematologic → normocytic, normochromic anemia due to low EPO

End Stage Renal Failure

the final stage of CKD

defined as GFR of less than 15

kidneys can no longer meet bodys needs

requires dialysis or transplant

Hemodialysis

separates waste and excess substances from blood using a semi permeable membrane

replenishes bicarb lost in the case there is metabolic acidosis

typical session lasts 3-6 hours and occurs multiple times a week

Dialyzer

artificial kidney

cylinder filled with thousands of tiny capillary tubes

Capillary Tubes

made of a semipermeable membrane that allows waste, electrolytes, and water to pass through but blocks blood cells and plasma proteins

Dialysate

fluid flowing on the outside of the tubes and pulls waste products out of blood by diffusion and osmosis

Heparin

added to the blood during dialysis to prevent clotting in the tubing

Hemodialysis Complications

hypovolemia → excess fluid removal can lead to dizziness, low BP, or shock

electrolyte shifts → rapid changes in K+, Ca2+, and other ions can cause arrhythmias or muscle issues

hemolysis → rare from mechanical stress or hypotonic dialysate

infection especially as vascular access sites

dialysis disequilibrium syndrome

Dialysis Disequilibrium Syndrome

most commonly during first dialysis session

over time urea builds up in the blood and slowly equilibrate with levels in neurons

dialysis quickly removes urea from blood creating a urea concentration gradient between blood and neurons

water rushes into neurons due to osmosis and can cause cerebral edema

Peritoneal Dialysis

catheter is surgically places into the peritoneal cavity to allow dialysate to enter and exit

dialysate contains glucose and electrolytes with a high osmolarity pulling excess fluid from the blood

lower electrolyte conc than blood promotes diffusion of waste into the dialysate

dialysate infused into peritoneal cavity and peritoneal membrane acts as filter, waste and excess fluid move from capillaries into dialysate

after a set time the fluid is drained → enough time for diffusion of solutes and osmosis of water

PD Types

CAPD (continuous ambulatory peritoneal dialysis) → preformed manually throughout the day

APD (automated peritoneal dialysis) → done at night with a machine

Dialysate PD

contains glucose to create an osmotic gradient that draws water out of the blood

infused into the peritoneal cavity

PD Goal

net negative fluid balance

more fluid drains out than was instilled, removing excess fluid from the body

PD Benefits

gentler on unstable patients → less hemodynamic stress compared to hemodialysis, for patients with low BP or cardiovascular instability

greater flexibility → allows patient to maintain more normal life bc it can be done at home, work, or while traveling

automated option available → automated peritoneal dialysis machine

Peritonitis PD

most common and serious complication of PD

caused by bacterial contamination during catheter handling or dialysate exchange

inflammation of peritoneum → abdominal pain, fever, nausea

can rapidly progress to sepsis if untreated

recurrent infections may scar the peritoneal membrane and impair dialysis → may require switching to hemodialysis

PD Complications

patient dependent → success depends on patient skill and hygiene bc its administered by patient

not appropriate for all patients because of certain abdominal conditions

peritoneal membrane failure → PD may stop working over time

storage challenges bc it requires home storage of fluids

body image concerns → catheters and abdominal distention can impact self image

CAPD

patient preforms 4-6 manual exchanges daily, draining used dialysate and infusing fresh solution into peritoneal cavity, no machine used only gravity and sterile technique

advantages → offers independence and flexibility, can be done at home, work, or traveling

challenges → higher risk of peritonitis from frequent catheter handling, requires patient adherence to regular schedule

APD

a machine preforms dialysis exchanges automatically usually overnight while the patient sleeps

advantages → convenient done at home with minimal daytime interruption, often better for working adults or kids

challenges → requires reliable equipment and power supply, less flexibility if traveling, machine maintenance and troubleshooting

AKI

sudden drop in renal function over hours or days

diagnosed by a rapid decline in GFR

progresses through 4 stages

often reversible if treated promptly

may progress to CKD if unresolved

pre renal → before kidneys

intra renal → in kidneys

post renal → after kidneys

Pre Renal AKI Causes

hypovolemia → hemorrhage, burns, dehydration, GI loss, trauma

cardiac → arrhythmias, cariogenic shock, HF, MI

peripheral vasodilation → antihypertensives

severe vasoconstriction → eclampsia (high BP damages renal vasculature), malignant hypertension (hypertensive crisis of over 180/over 120)

Intra Renal AKI Causes

most common is acute tubular necrosis

caused by ischemia (prolonged low blood flow from sepsis, dehydration, HF) or nephrotoxins

dead tubular cells slough off and block tubules

causes back lead of filtrate into blood through damaged epithelium

impaired reabsorption and secretion → fluid, electrolyte, and acid base imbalances

lower GFR due to tubular obstruction and waste accumulates in the blood

Nephrotoxins AKI

NSAIDs → inhibit prostaglandins and causes afferent arteriole constriction, lowers peritubular capillary blood flow and causes ischemic tubular injury

aminolycosides → directly toxic to PCT and triggers cell death

myoglobin → released during rhabdomyolysis and filtered by kidneys, directly toxic to tubule cells and can obstruct tubules

Post Renal AKI Causes

bladder outlet obstruction → benign prostatic hyperplasia, bladder tumors, and anticholinergic meds that impair bladder emptying

urethral obstructions → kidneys stones lodged in ureter or urethra, or urethral stricture (scarring from infection or injury)

neurogenic bladder → nerve damage disrupting bladder emptying and causing urinary retention

BUN Creatinine Ratio

normal ratio is 10:1 or 20:1

both are freely filtered by the glomerulus

creatinine is not reabsorbed or secreted

urea (BUN) is reabsorbed so it rises faster than creatinine in kidney disorders

helps differentiate types of renal dysfunction in AKI

Pre Renal BUN Creatinine Ratio

large BUN Creatinine Ratio

urea is reabsorbed especially when filtrate moves slowly (low GFR)

creatinine is still not reabsorbed

slow flow means more time for urea reabsorption → BUN increases more than creatinine

result → both rise, BUN more

Intra Renal BUN Creatinine Ratio

small increase in BUN Creatinine Ratio but usually still in normal range

both urea and creatinine are freely filtered across glomerulus

less urea reabsorbed due to death of tubular cells

Post Renal BUN Creatinine Ratio

in early AKI backpressure slows filtrate flow leaving more time for urea reabsorption

BUN rises more than creatinine

if prolonged the tubular damage reduces reabsorption and both BUN and creatinine rise and ration returns to normal

post renal AKI may initially mimic pre renal but ratio normalizes as tubular injury develops

AKI Initiation

lasts hours to days as injury occurs

onset of injury → phase begins with this

asymptomatic or minimal symptoms → patient may have no symptoms and initial lab tests may only show subtle changes (hard to detect)

AKI Oliguric

typically lasts a few days to weeks

low urine output often less than 400

waste buildup → high BUN and creatinine, low creatinine clearance

biggest problem → uremia causing seizures, coma, death

fluid overload → pulmonary/peripheral edema, HTN, HF

electrolyte imbalance → hyperkalemia, metabolic acidosis

AKI Diuretic

recovery begins and typically lasts 1-2 weeks

increased urine output (polyuria) and waste excretion resumes with BUN and creatinine declining as kidneys regain function

risk of dehydration → high urine output can deplete fluid

electrolyte imbalances → especially hypokalemia and hyponatremia due to urinary loss

AKI Recovery

lasts several weeks to months

gradual improvement in kidney function and normalization of labs

serum creatinine and BUN levels trend back to normal

urine output stabilizes

electrolyte balances are restored

if AKI doesn’t improve CKD can develop