N323 - Week 8 (Renal Pathophysiology)

Glomerulus

receive 1000 to 2000 mL of blood per min, does filtration

Glomerular filtration rate (GFR)

The filtration of the plasma per unit of time

-high hydrostatic pressure necessary to push blood through the filtration process

Kidney

regulated by CNS (specifically by autonomic nervous system)

-Sympathetic: fight or flight (hold in pee)

-Parasympathetic: relaxation (urinate)

Kidneys are regulated by...

Neural regulation

Hormones

Neural Regulation of kidney

Sympathetic fibers regulate size of afferent & efferent arterioles (renal blood flow)

-Micturition Reflex

Afferent & Efferent Arterioles

afferent: arterioles: toward the kidneys

efferent arterioles: exit the kidneys

Micturition Reflex

reflex that controls when we urinate & allows us to urinate

-stretching of tissue -> senses fullness -> smooth muscle contracts (internal urinary sphincter opens) -> urge to urinate but can control it (voluntary control of urination)

Hormones of Kidneys

Renin-angiotensin-aldosterone system (Major regulator of renal blood flow)

Renin-angiotensin-aldosterone System (RAAS)

low BP -> renin is released from the kidneys ->

renin will transform angiotensinogen (from the liver) into angiotensin I (inactive) ->

ACE (angiotensin converting enzyme produced in lungs) converts angiotensin I into angiotensin II ->

stimulates release of aldosterone (from adrenal glands) ->

causes reabsorption of NaCl & H2O

Angiotensin II

causes vasoconstriction

Goal of RAAS

increase blood volume and blood pressure

Nephron Functions (4)

filters plasma at glomerulus

-tubular reabsorption & secretion

-forms a filtrate of protein-free fluid

-regulate the filtrate to maintain fluid volume, electrolytes & pH

Kidney & glucose regulation

does gluconeogenesis

-reabsorbs glucose from glomerular filtrate (though SGLT2)

-takes up glucose from circulation

-stimulated to release glucose by epinephrine & inhibited by insulin in both kidneys & liver

Sodium-glucose cotransporter 2 (SGLT2)

reabsorbs glucose from the glomerular filtrate

Parts of Nephron (6)

glomerulus (capillaries of filtration) ->

bowman's capsule ->

proximal convoluted tubule ->

Loop of Henle (descending & ascending loop of Henle) ->

distal convoluted tubule ->

collecting duct

Antidiuretic hormone (ADH) (4)

necessary for reabsorption of water in the collecting ducts

-determines the final concentration of urine

-secreted from the posterior pituitary

-increases water permeability & reabsorption in the tubule

Pediatric renal function

decreased ability to remove excess water & solutes

-decreased concentrating ability

-narrow margin for fluid & electrolyte balance

-increased risk of drug toxicity

Aging & renal function

decrease in renal blood flow & GFR (altered Na & H2O balance)

-# of nephrons decrease (due to renal vascular & perfusion changes)

-response to acid-base changes delayed

-increased risk for drug toxicity

-alterations in thirst & water intake

Forms of Upper Urinary Tract Obstruction (4)

hydroureter

-hydronephrosis

-Ureterohydronephrosis

-kidney stones (nephrolithiasis)

hydroureter

accumulation of urine in the ureter

hydronephrosis

enlargement of the real pelvis & calyces

Ureterohydronephrosis

dilation of both the ureter & the pelvicaliceal system

Kidney stones (nephrolithiasis) (3)

calculi or urinary stones

-masses of crystals, protein or other substances that form within & may obstruct the urinary tract

-classified according to the minerals that make up the stone

Clinical manifestation of Kidney Stones

Renal colic

Renal colic (3)

pain related to spasms of smooth muscle in ureter

-can radiate from lower flank to groin

-moderate to severe pain

Evaluation of Kidney Stones (3)

imaging studies

-24-hour urinalysis

-pain control

Urinary tract infection (UTI)

inflammation of the urinary epithelium caused by bacteria

-most common cause of UTI is E.coli

Acute cystitis (uncomplicated)

inflammation of the bladder

-most common site of UTI

Painful bladder syndrome/interstitial cystitis (3)

pain, discomfort or pressure of bladder that lasts longer than 6 wks, can have ulcerations

-absence of infection (alrdy been treated), no identifiable causes

-common in middle aged women

Acute Pyelonephritis

acute infection of the ureter, renal pelvis, interstitium

-caused by vesicoureteral reflux (any backflow of urine) -> high risk of infection

-common in babies

Chronic pyelonephritis (2)

persistent or recurring episodes of acute pyelonephritis that lead to scarring (permanent damage to kidneys)

-risk increases in individuals w/ renal infections & same type of obstructive pathologic condition

Causes of Glomerulonephritis (3)

type III hypersensitivity - Deposition of circulating soluble antigen-antibody complexes, often w/ complement fragments

-type II hypersensitivity (attach to tissue) - antibodies reacting in situ against planted antigens w/in the glomerulus

-nonimmune (drugs, toxins, ischemia)

2 Major symptoms of Severe Glomerulonephritis

Hematuria w/ RBC casts

-Proteinuria exceeding 3-5 g/day w/ albumin (macroalbuminuria) as the major protein

Other symptoms of Severe Glomerulonephritis (3)

oliguria (decreased urine output)

-hypertension

-edema

3 phases of Acute Kidney Injury (AKI)

1. Initiation Phase

2. Maintenance (oliguric) phase

3. Recovery (polyuric) phase

Initiation Phase of AKI (2)

kidney injury is evolving

-prevention of injury is possible

Maintenance (Oliguric) Phase of AKI (3)

established kidney injury & dysfxn

-urine output is lowest during this phase

-serum creatinine and urea nitrogen both increase in blood

Recovery (polyuric) Phase of AKI

injury repaired & normal renal fxn established

-diuresis common

-decline in blood serum creatinine & urea (increase in creatinine clearance)

Chronic kidney disease (CKD)

progressive loss of renal fxn that affects nearly all systems

-associated w/ HTN, diabetes, intrinsic kidney disease

*GFR Stages

normal (GFR>90)

Mild (60-89)

Moderate (30-59)

Severe (15-29)

End stage (

Process of Chronic Kidney Disease

Renal injury ->

loss of nephrons -> angiotensin II ->

glomerular capillary HPT ->

glomerular permeability & filtration increases ->

proteinuria ->

tubular protein reabsorption increases ->

tubulointerstitial inflammation & fibrosis ->

renal scarring ->

systemic hypertension & more loss of nephrons

CKD & Impact on Fluid & Electrolyte Balance

affects..

-sodium & water balance

-potassium balance

-acid-base balance

Sodium & water balance in CKD

sodium excretion increases w/ obligatory water excretion leading to sodium deficit & volume loss

-concentration & dilution ability diminishes

Potassium balance in CKD

tubular secretion of K increases early

-once oliguria sets in, K retained

Metabolic acidosis

when GFR is 30%-40%