PATHO 5: Renal

renal system: overview

maintains internal homeostasis by regulating fluid balance, electrolytes, acid-base status, and bp

removes metabolic waste products (like urea, creatinine) & toxins from the blood through urine formation

anatomy of kidney

cortex: outer layer, contains glomeruli

medulla: inner region with renal pyramids

renal pelvis: collects urine into ureter

nephrons: microscopic functional units

review of nephron: globalmerulus

network of capillaries that filter blood

high pressure system forces water, electrolytes, glucose, & waste into the nephron

proteins & blood cells too large to pass

review of nephron: bowmans capsule

surrounds glomerulus, collects filtered particles, & funnels it into proximal tubule

review of nephron: proximal tubule

65-70% of filtrate reabsorbed

- reabsorbs water, nutrients

- secretes H+

review of nephron: loop to henle

concentrates urine

descending limb: highly permeable to water, not to solutes --> water leaves into medulla

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

review of nephron: distal tubule

reabsorbs sodium (Na+) under influence of aldosterone

excretes potassium (K+) and hydrogen ions (H+) --> helps with electrolyte & acid base balance

review of nephron: collecting duct

collects fluid from multiple nephrons

responds to adh here (increased adh = increased water reabsorption)

genitourinary system overview: function

ureters: tube that allows urine to travel from kidneys to bladder

bladder: storage of urine

micturition: act of urination

- unidirectional flow of urine (with gravity)

- urination has a lavage (flushing) effect that helps clear bacteria from the urinary tract, reducing the risk of infection

urethra: exit point for urine to leave body

clinical assessment of renal function

urinary output

- at least 30 mL/hr

alterations in urine output

- oliguria --> <30 ml/hr (<400 ml/day)

- anuria --> no urine

- nocturia --> increased urination at night

blood tests

- serum creatinine

- waste product from muscle metabolism

- blood urea nitrogen (BUN)

- reflects protein metabolism; rises with decreased kidney function of dehydration

- gfr

- measures how well kidneys filter blood; a lower gfr indicates reduced kidney function

- best measure of overall kidney function

GFR & creatinine are inversely related

clinical assessment of renal function cont

urinalaysis

- visual, chemical, microscopic analysis

- ph, specific gravity, protein, glucose, ketones, nitrites, rbcs

protein-creatinine ration

specific gravity --> urine density (ability to concentrate/dilute urine); 1.003 - 1.030

kidney, ureter, bladder (kub), xray

ultrasound

ct/mri

common clinical manifestations of kidney dysfunction

pain

- lower urinary tract

- kidney (nephralgia)

- cva tenderness/flank pain

abnormal ua

- color, odor, tubidity

- hematuria

dysuria, urgency, frequency

oliguria

urinary tract infections

inflammation of the urinary epithelium following invasion and colonization by a pathogen within the urinary tract

- escherichia coli (80%) is most common pathogen

uropathogens overcome host defense mechanisms

- mucus

- micturition with unidirectional flow

- epithelial cells/inflammation

uti risk factors

female gender, pregnancy

diabetes mellitus

urinary obstruction

indwelling catheters (foley)

uti etiology

ascending infection/inflammation

urine stasis

bacteremia

uti clinical manifestations/evaluation

dysuria, frequency, urgency

hematuria, turbid ua

fever, chills, cva tenderness

urinalalysis, culture & sensitivity

older adults: confusion

uti treatment

antibiotics

fluids

urethritis

inflammation of urethra

sti (gonorrhea & chlamydia)

cystitis

inflammation of bladder

many cuases, bacterial infections most common

pyelonephritis

inflammation or infection of kidneys

urinary tract obstruction

blockage of urine flow within the urinary tract

- obstruction can be caused by an anatomic or functional defect

- obstructive uropathy

severity based on:

- location

- completness

- involvement of one or both upper urinary tracts

- duration

- cause

renal calculi (nephrolithasis/kidney stones)

masses of crystals, protein, or other substances that form within and may obstruct urinary tract

risk factors:

- male sex

- aged 20 - 40

- inadequate fluid intake

- dietary factors (i.e. calcium intake)

kidney stone

supersaturation of one or more salts

- presence of a salt in a higher concentration that the volume able to dissolve the salt

precipitation of a salt from liquid to solid state

- temperature and ph

grows into stone by crystalization or aggregation

composition of mineral salts

- calcium oxalate/phosphate (75-85%)

- struvite (magnesium, ammonium, phosphate: 10%)

- uric acid (7%)

kidney stone manifestations

renal colic (spasmodic pain caused by kidney stone)

- flank pain that radiates

hematuria --> gross or scant amounts

kidney stone evaluation

kidney-ureter-bladder (KUB)

abdominal computed tomography (ct)

stone analysis

intravenous pyelogram

kidney stone treatment

stone removal

pain management

fluids

dietary decrease based on stone type (i.e. calcium)

urinary tract obstruction complications

dilation of the tract proximal to the obstruction

- hydroureter

- hydronephrosis

urinary stasis causes risk for uti

prolonged obstruction --> postrenal acute kidney injury and acute tubular necrosis

bilateral obstruction

- fluid retention

partial obstruction

- compensatory hypertrophy in inaffected kidney

glomerular disorders

alterations in structure/function of the glomerular capillary circulation

- can be sudden or insidious onset

- acute glomerulonephritis

- nephritic & nephrotic syndrome

glomerular disorder pathophysiology

glomerular damage causes decreased glomerular membrane surface area & capillary blood flow

decreased glomerular filtration rate

- elevated plasma creatinine, urea, & reduced creatinine clearance

increased glomerular capillary permeability --> plasma proteins leak into the urine

hypoalbuminemia encourages plasma fluid to move into the interstitial spaces

acute glomerulonephritis

inflammation of the glomerulus

- triggered by bacterial, viral, parasitic, systemic causes

- immunologic abnormalities (most common)

- e.g. post infectious acute glomerulonephritis (sometimes after infection those antibodies get stuck in kidney filters and cause inflammation)

- group a b-hemolytic streptococci (strep throat)

AG pathophysiology

formation of immune complexes in the circulation deposit in

glomerulus: this is a type III hypersensitivity reaction

- antibodies produced against strep initiate glomerular inflammation and injury (may be related to inadequately treat strep)

activation of complement system

recruitment/activation of immune cells and mediators --> inflammatory response in glomerulus

AG clinical manifestations

decreased gfr

- decreased glomerular blood flow due to inflammation

- increased BUN and creatinine

- glomerular necrosis (scarring)

- glomerular basement membrane thickens

- increased permeability to proteins

hypertension

hematuria

- smoky, brown-tinged urine

- rbc cells

proteinuria

- low serum albumin

- edema

eventual oliguria

- oliguria: urine output <30 ml/hr or <400 ml/day

AG evaluation

H&P, UA

BUN & creatinine levels

renal biopsy

AG treatment

supportive & symptomatic

usually resolves with minimal treatment (especially if poststrptococcal infection); however may progress to chronic case or nephrotic syndrome

dialysis with worsening disease

nephrotic syndrome

kidney disorder caused by non inflammatory damage to the glomerulus & basement membrane/podocytes

- kidneys "filter mesh" is being attacked from the outside

damage leads to:

-protein loss in urine (proteinuria),

which results in hypoalbuminemia (low albumin serum), decreased oncotic pressure (edema), & compensatory hyperlipidemia (lipiduria)

nephrotic syndrome findings

excretion > 3.5g protein in the urine per day

nephrotic syndrome etiology

glomerulonephritis

defects that alter the glomerular membrane (genetic)

systemic diseases (diabetes, sle)

drug/toxin injury (nsaids)

infections (especially chronic and/or recurrent)

nephrotic syndrome pathophysiology

non-inflammatory glomerular damage increases permeability, allowing large proteins (albumin) to leak into urine (gross proteinuria)

loss of albumin reduces plasma oncotic pressure (edema)

liver compensates for hypoalbuminemia by increasing lipoprotein synthesis (hyperlipidemia)

damaged glomeruli allow lipoproteins to pass into the urine, leading to lipiduria

nephritic syndrome

caused by immune mediated inflammation of the glomeruli

- capillary wall is being attacked from the inside

leads to damaged capillary walls that allow rbs & some protein to leak into the urine, resulting in hematuria, mild proteinuria, htn, and decreased gfr

nephritic syndrome etiology

post streptococcal glomerulonephritis

lupus nephritis (autoimmune disease that attacks the body)

iga nephropahty (bergers disease: leads to deposition of iga antibodies in glomerulus & inflammatory immune response)

nephritic syndrome pathophysiology

inflammation of the glomeruli damages the glomerular capillary wall

leads to reduced glomerular filtration rate (gfr) --> oliguria

rbcs & proteins leak into urine d/t increased membrane permeability --> mild proteinuria & hematuria

sodium & water retention leads to htn & edema

renal failure: acute kidney injury (acute renal failure)

sudden and rapidly progressive within hours (often reversible); abrupt reduction in renal function

disruptions in fluid, electrolyte, acid/base balance, waste excretion, gfr

renal failure: chronic kidney disease (chronic renal failure to end stage kidney disease)

chronic, slowly progressing to end stage renal failure over months or years

progressive & irrevocable loss of nephrons

AKI types: prerenal

caused by impaired blood flow

- sudden reduction of renal perfusion (shock)

gfr declines due to the decrease in filtration pressure --> oliguria

ischemia leads to hypoxic injury & acute tubular necrosis (atn) if renal perfusion < 20%

AKI types: intrarenal

damage to the renal parenchyma

acute tubular necrosis

- ischemia (prolonged prerenal failure, sepsis)

- nephrotoxic (contrast dye, rx)

- vascular

- inflammation, reperfusion injury

- glomeular

- acute glomerulonephritis

- interstitial

- acute pyelonephritis

AKI types: postrenal

occurs with urinary tract obstructions that affect the kidneys bilaterally & increase the intraluminal pressure upstream

atn develops if injury uncorrected in a few hours

acute tubular necrosis clinical presentation

prodromal (initiation) phase

- normal or declining urine output

- rising bun & creatinine

oliguric (maintenance) phase

- decreased urine output

- increased bun and creatinine (& other waste products)

- increased water retention

- metabolic acidosis & hyperkalemia

postoliguric (recovery) phase

- beginning of renal recovery

- diuresis

- decreased bun & creatinine

AKI clinical manifestations

oliguria/anuria

elevated bun & creatinine

- axotemia: decreased urea and frequently creatinine levels

- uremia

- elevated urea & creatinine levels

hyperkalemia

metabolic acidosis

hypertension (volume overload)

AKI treatment

identify at risk patients

- prevent development

- address hypotension/hypovolemia

- decrease invasive procedure (catheters)

- careful use of contrast solution

- treat early

- enhance renal perfusion before atn develops

- aggressive management of glomerulonephritis

recovery 1 week to 1 year

chronic kidney disease (CKD leading to ESRD)

the irreversible loss of renal function that affects nearly all organ systems

diabetes and htn primary risk factors

findings

- decreased kidney function for 3+ months based on blood tests, UA imaging, gfr (<60 ml/min)

stages of CKD by nephron loss: decreased renal reserve

< 75% nephron loss

no s/s

bun & creatinine normal

stages of CKD by nephron loss: renal insufficiency

75-90% nephron loss

polyuria (can't concentrate urine)

slight bun/creatinine elevation

stages of CKD by nephron loss: end stage renal failure

hemodialysis required

> 90% nephron loss

azotemia/uremia

anemia

f/e abnormalities

CKD clinical manifestations

kidneys have an impact on many body systems

- htn & cardiovascular disease

- anemia

- uremic syndrome

- metabolic acidosis

- electrolyte imbalances

- mineral & bone disorders

- malnutrition

- pain

- depression

htn/cardiovascular disease

htn/cv disease

- htn, chf can result:

- volume overload, hyperactivity of raas

- atherosclerosis, dyslipidemia, anemia, dysrhythmias

anemia

lack of erythropoietin (epa)

uremia creates a toxic environment for rbcs

cardiorenal anemia syndrome

- worsening ckd, anemia, hf

CKD: mineral & bone disorders

hypophosphatemia

hypocalcemia

hyperparathyroidism

- brittle bones & vit d cant activate

skin changes

- bruises

- itching

- uremic frost

- yellowing

CKD management

monitor bun & creatinine

monitor gfr

systemic assessment

CKD clinical management

slow progression to ersd & manage complications

htn --> goal 130/80

dm

acidosis

fluid & electrolyte balance

anemia

- erythropoiesis stimulating agents improve qol

CKD treatment: dialysis

planning stage 4

indicated at stage 5

required when:

- uremia

- hyperkalemia unresponsive to other treatment

- severe volume overload

hemodialysis

peritoneal dialysis

transplant