RENAL

Definitions
Anuria: none/<50-100mL in 24 hr
Polyuria: large amts/volume (?>3L/24hr)
Frequency: more than q2hr
Dysuria: painful voiding
Micturition: voiding
Hematuria: blood in urine
Proteinuria: protein in urine
Glycosuria: glucose in urine
Stress incont: activities induce-cough,laugh,sneeze
Uremia

Oliguria: <400mL/24 hours (low output)

Urgency: sudden strong desire to void (can control)
Nocturia: >2/night
Enuresis: bedwetting
Incontinence: involuntary loss of urine
Residual/urinary rtn: urine left in bladder after void
Hesitancy: delay of ignition (10 seconds)-needs
abdominal pressure to void
Uremic fetor
Azotemia

A&P
Kidney: sits in retroperitoneal space (flank); enclosed renal capsule; left above right; 25% CO goes through-1L/min
Ureter: 25-30cm; urine bladder
Bladder: muscular 3-lyr bag (inner longitudinal, middle circular, outer long.); sphincterurethra 300-600mL
Urethra: male-20 cm; women-2-4 cm
Aging: (1) slowing GFR; (2) becomes funnel shaped; (3) bladder wall weaken
Micturition: bladder fillstriggers PNSspinal cordexternal sphincter relaxesperson voids; avg: 8times/24hr
Nephron: functional unit of kidney; 1 million/kidney; 1L enter through each nephron-125mL/min(GFR)only 1% urine
20-25% COrenal arterybowmans capsuleglomerulusfilter (lytes); not large stuff (RBC, WBC, prot., platelet)
Functions of Kidney: (maintenance of overall homeostasis)
controls F&E
controls acid base
regulates BP (RAAS)
prostaglandin synthesis insulin degradation
calcium/phosphorus reg

erythropoietin production
vitamin D metabolism

Effect of aldosterone sodium retention (water); ADH conserve fluid

Diagnostic Tests
24 hour urine collection:
lytes, hormones, meds, creatinine [CrClcan get serum/24 hr urine, compare = GFR)
nursing: set up reminders, discard initial void at 0800save all urine including last void at 0800
Serum tests
BUN: urea = end product of protein metabolism (can also increase w/ high protein, starvation, dehydration)
Creatinine: end product phosphocreatinine met. (protein waste)can be muscle disease; incr when 50% function lost
ratio = 10:1
Radiological Studies
KUB (kidney, ureter, + bladder radiograph): form, size, position kidneys; no contrast; bowel prep if ordered
Flat plate of abdomen: kidneyshydronephrosis; stones can stand out
CT: visualization of kidneys/masses; iodine sensitivity?
MRI: visualize kidneys; not reliable det. calculi/tumours
Scan: blood flow, GF, tubular fxn, excretionradioactive isotopes/proves
Ultrasound: renal/prerenal masses; *safe with renal failure!
Intravenous Pyelogram (IVP): allows visualization of urinary tract after IV contrast material (radiographs taken
sequentially through UT)
o Before: (1) consent (2) iodine/shellfish allergy (3) bowel prep (pm before) (4) NPO 8 hours (5) assess renal
function (BUN/Cr)dye wont be excreted; can be nephrotoxic
o Alert to: facial flushing, salty taste with dye; Post test: push fluids, monitor output, VS (anaphylactic rxn)
Endoscopy: Cystourethroscopy/Cystoscopy *sometimes can go up into ureters?
Lithotomy positionlegs up; meatus cleaned; very quick
*dont do if infxpush bacteria up higher

 Force fluids, observe for clots/hematuria (damage intima), UTI; meatus may hurtsitz bath/NSAIDS
*CT, MRI, bladder scan, ultrasoundfull bladder? which is safe with renal failure? Why assess renal fxn before IVP?
CYSTITIS (lower UTI/inflammation of bladder)
Most common bacteria: E.Coli! 80% (rel. to rectum?); klebsiella, proteus, serratia, enterobacter, pseudomonas
Other causes: fistula between intestine/bladder, catheter, neurogenic bladder pt w/ infxn
*Common Rx: sulfonamides
Risk factors:
Women 8x more Pregnanc Post-minnow (hormones flux)
Nosocomial infxn (caths)
y
Poor hygiene
Thongs
Old men (not emptying-BPH)
DM (neuropathy prevents emptying
Signs and Symptoms:
Urg/freq
Malaise
Cloudy urine Abd/flank pain
Incomplete emptying
Dysuria
Hematuria
Itching
Lowback/suprapub pain
Inability/small amts void
*OAs: confusion/mental status change

Def
Cause
S/Sx

Dx

RENAL INFLAMMATION/UPPER UTI

PYELONEPHRITIS (one side)
GLOMERULONEPHRITIS (both sides)
Inflamm process (renal pelvis/surrounding tissue
Inflamm process (proliferative/infl changes of
hylum)
glomeruli accompanied by tubular, interstitial and
vascular changes)
Bacteria (E-COLI!); cystoscope, catheter
Immune rxn (nephrotic/nephritic syndromes; strep)
Fever, chills, weak, pallor, NV, ha, anorexia
Fever, chills, weak, pallor, NV, ha, anorexia
Abdominal/flank pain on affected side
HTN (moderate to severe)
Dysuria, freq, urg, hematuria, foul/cloudy pee
Decreased visual acuity
Generalized edema (facial, periobital)
Oliguria, anuria, hematuria, proteinuria(foamy)
insidious or sudden, can lead to chronic glom or
ESRD, can take up to 2 yrs to recover
(1) Urinalysis [cloudy, WBC, casts, bacteria, hemat] (1) Urinalysis/Serum [BUN, Cr/CrCl, Crea protein,
(2) Urine C&S [whats growing?]
foamy, Hgb, Hct]
(3) KUB, IVP, MRI, CT
(2) Antistrep titer
(3) Renal biopsy
Nephrotic Syndrome:
set of s/sx caused by protein loss (wasting) secondary to diffuse glomerular damage

3 SYMPTOMS: (1) proteinuria (2) hypoalbuminemia (3) edema

- Protein loss in urine = altered oncotic pressure = interstitial fluid shift = edema; low CV volume stimulates RAAS
causing retention of Na+ and H2O=large accumm in ECF = edema
Causes:
- Glomerulonephritis - SLE - HF - Hep B - DM - Renal vein thrombosis
-Allergic rxn -SCA
-*Most common = strep throat (Group A beta hemolytic) *if not treated, it can circulate through body and start to
accumm on heart valves and glomerulus/rheumatic fever
Nephritic Syndrome:
Antigen-antibody (immune) complex get trapped in glomerulusformed elsewhere in body but trapped in filtering
processcauses inflammatory damage (things can get out-into pee) and reduced glomerular function
Set of S/Sx that includes hematuria and 1 or more of:
Incr BUN Dec. GFR Oliguria[glom damaged = dcr GFR]
Causes: - Immunoglobulin A nephropathy

-Henoch-Schontein purpura

HTN [dcr GFR=dcr filtrat/output]

URINARY CALCULI
Urolithiasis: stones in urinary tract (usually ureters)
Men > women; 20-55 yrs
Nephrolithiasis: stones in kidney
Tend to recur (50% in 5 years)
Causes:
- urinary stasis
- dehydration
- supersat of urine w/ poorly
- high Ca+ diet
- high mineral h2o
- UTI
- neurogenic bladder
soluble crystalloids
Patho:
Unknown, crystals form + growth continues (aggregation to larger particles) stones can be small or big
Types:
Calcium (90%): immobile, cancer, Ca+ leaks out of bones, decrease gut absorp, high diet, impaired tubular resorp
Oxalate: inflammatory bowel disease; too much vit C
Struvite: form in alkaline urine-bacteria?
Uric acid: gout? Diets high in purinesaffinity for toe-ear, heart, kidneys
Cystine
S/Sx
Complications
Pain (colic)
Pain, spasm, colic (peristalsis)
Kidney (flank, radiates to testicles or bladder)
Obstruction (hydroureter/nephrosis)
Ureter (flank, radiates to genitals or thighs)
Tissue trauma (bleeding)
Fever, Incr WBC
Infection (stasis)
Pain stimulates ANS, so you may see:
Diagnostic Tests
NV, pallor, grunting resps, incr. BP/HR, diaphoresis
Serum uric acid*
Ultrasound
Urinary Alterations
KUB
Cystoscopy
Oliguria, anuria, freq, change in stream, Hematuria
IVP
CHRONIC KIDNEY DISEASE
Progressive, irreversible destruction of nephrons in both kidneys ( renal fxn)
Risk Factors
- age - ethnicity (aa, abor, his, asia) - family Hx - low income/edu - HTN - DM - drug tox -autoim -UTI/sys infx
Causes (*diabetes = # 1; HTN = # 2 cause of ESRD)
Diabetes (34%)
HTN
Chronic glomerulonephritis Obstruction (calculi
AKI (not resp. to tx)
Nephrotoxins
Chronic infxn (pyelonephri) Autoimmune (lupus)
Pathophysiology
Deteriorationremaining functioning neurons hypertrophyoverburdenedbecome sclerotic/thickdestruction
*Lose their ability to concentrate (dilute urine) and cant absorb lytes (increasing sodium in urine)
Total GFR and clearance leading to BUN and creatinine
Sx of Uremia (if CKD continues unchecked = uremic toxins = fatal changes to all systems)
Ocular: retinopathy, red eye
Endo: hypothyroidism, hyperparathyroidism
Resp: uremic lung, pleuritis, pulmonary edema
CV: CHF, HTN, pericarditis
GI: NVDA, bleeding, uremic fetor*
Hemat: anemia, bleeding, risk infxn
Derm: pallor, pruritis, dry, sweat, yellow-grey, dry hair
Repro: infert, libido, impoten, amennorhea, delayed pub
Metab: acidosis, hyperglyc, hypertriglyc, hyperuricemia
Neuro:fatigue/drow, depress, periph neuropathy, insomnia
Msk: renal osteodystrophy, malacia, sclerosis, osteitis, soft restless leg
tissue calcification, retarded growth
*uremic fetor-breath-urine/ammonia-bitter/metallic taste
Diagnostic Tests *might do these regularly to monitor
Hx, physical exam
Renal US/Scan
Urinalysis/culture
Renal Biopsy
Serum Cr., BUN, CrCl, lytes
Uremic frost (urea crystalizing on
CT/MRI
Hgb/Hct
skin = BUN ++
5 Stages of CKD
Normal/@ risk: >90

Stage 1:
Stage 2:
Stage 3:
Stage 4:
Stage 5: *ESDR

>90
60-89
30-59
15-29
<15

Kidney damage (protein in urine); normal/high GFR

Damage/mild decrease
Moderate decrease
Severe decrease
Kidney failuredialysis or transplant needed

*$/edu risk factor/nephrons in both kidneys/?uremic fetor; nephs lose ability to dilute/conc?cant absorb lytes incr/decr Na+ in urine

ACUTE KIDNEY INJURY (oliguric = higher mortality)

Prerenal: blood flow glom perfusion and filtration [55-60%]
Hypovolemia: severe hypotension, D/V, excessive diuretic use, burns (third spacing) **fix problem ex. push fluids
CO: HF, MI (not getting enough fluid through renal artery)
peripheral vascular resistance
Renal vascular obstruction: embolus, etc. blocking renal artery
* AKI r/t prerenal causes is usually reversibleif cause prolonged, intrarenal damage may occur, leading to ATN
Intrarenal: direct damage to renal parynchyma (tissue), resulting in impaired nephron function [35-40%]
Prolonged ischemia
Nephrotoxins: (1) AMINOGLYCOSIDESgram negativegentamycin (2) NSAIDs (3) ACE inhibitors
Acute glomerulonephritis
Systemic lupus (SLE)
Interstitial nephritis (allergies, infection)
*can lead to ATN (caused by ischemia, nephrotoxins+pigmentslike heme, myoglobins, etc.)
Postrenal: mechanical obstruction of urinary outflow [5%]
BPH
Calculi
Strictures
Trauma
Prostate cancer
Extrarenal tumours
ACUTE TUBULAR NECROSIS
2 most common causes of AKI which lead to ATN are:
1. PROLONGED RENAL ISCHEMIA: disrupts basement membrane with patch destruction of tubular epithelium
2. NEPHROTOXIC INJURY: direct necrosis of tubular epithelial cells which slough off and plug tubules
Pathological processes
1. Hypovolemia + renal BF RAAS constrict. of arteries [periph/renal afferent] bf, tubular dysfunc, oliguria
2. Ischemia alters glom. epi cells + glom capillary permeability bf, tubular dysfunc
3. Damaged tubules cause interstitial edema + necrotic cells accumm. in tubules GFR (obstruc intratubular press.)
4. Glomerular filtrate leaks back into plasma intratubular fluid flow
Clinical Manifestations and Phases
1. INITIATION: time of insult to apparent s/sx
urine output
BUN and Cr
2. MAINTENANCE: days-weeks (oliguric phase)
Urinary changes:
FVE:
Met. Acidosis
- Oliguria (<400mL)
- JVD, HTN
- Kaussmaul
- SG 1.01 (dilute-close to H2O) - bounding pulse - Lethargy/stupor
- High Na+
- edema
- RBCs, WBCs, proteinuria
- CHF, p. edema
- Acidosis-hydrogen ions
- cerebral edema

Lytes/waste
- Na+
- Ca2+
- K+
- PO4- BUN/Cr

Neuro
- fatigue
- diff concen
- seiz/coma
- stupor

Hemat
- anemia
- bleeding
- immunodef
- infxn?

3. RECOVERY: begins when GFR starts to (osmotic diuresis!)

(*may take 3-12 months to stabilize renal fxn)
Osmotic Diuresis: daily output 1-3 L/day++; kidneys can excrete waste but not concentrate = dilute uring
o Complications: hypotension, hypovolemia, hyponatremia, hypokalemia, dehydration
Blood Values: GFR allowing BUN/Cr levels to plateau then
*OAs less likely to recoverdevelop chronic

Diagnostic Tests (AKI)

- CrCl
- Serum Cr/BUN
- Urinalysis
- CT-no MRI!

- Serum lytes
- Renal US
- Renal scan
- Hx (cause? Pre? Intratakes longer/less likely to recover! Post?)