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Alterations of Renal and Urinary Tract Function Chapter 28, 29
35

Renal Pathophysiology

Jan 17, 2016

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Page 1: Renal Pathophysiology

Alterations of Renal and Urinary Tract FunctionChapter 28, 29

Page 2: Renal Pathophysiology

Structures of the Renal System

2

Page 3: Renal Pathophysiology
Page 4: Renal Pathophysiology

Kidney FunctionFluid and electrolyte balance

Regulation of blood pressure

Excretion of metabolic wastes

Acid/base balance

Erythropoietin production

Vitamin D activation

4

Page 5: Renal Pathophysiology

Nephron-Functional Unit

5

Page 6: Renal Pathophysiology

Urinalysis– Color– Specific gravity– Protein– Glucose– Ketones– Nitrites– Casts– Crystals– pH

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Page 7: Renal Pathophysiology

Hematologic Tests

• GFR mL/min [eGFR] 125/min

• Serum Creatinine 0.6-1.2 mg/dL

• BUN 10-20 mg/dL

7

Page 8: Renal Pathophysiology

Bladder Disorders

• Incontinence

– Requires physiological and cognitive capabilities• Need functioning nervous system, intact bladder and

urethral function

8

Page 9: Renal Pathophysiology

Incontinence

• Define the following types of incontinence– Stress

– Urge

– Mixed

– Overflow

– Functional

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Page 10: Renal Pathophysiology

Enuresis

• Inappropriate wetting of clothes or bed

– Primary cause is maturational delay

– Diurnal vs. nocturnal

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Page 11: Renal Pathophysiology

Urinary Tract Obstruction

Page 12: Renal Pathophysiology

Kidney Stones, Renal Calculi, Nephrolithiasis

• Etiology– Factors influencing formation

• Increased concentration of solutes• Abnormal urine pH• Low urine volume• Hypercalciuria• Genetic predisposition

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Page 13: Renal Pathophysiology

Kidney Stone

• Clinical Manifestations– Vary with size and location

• Abdominal pain• Flank pain• Ureteral colic• Hematuria• Dysuria

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Page 14: Renal Pathophysiology

Entry of Pathogens

14

Normal Defenses

Acidic urine and urea

Unidirectional Flow

Voiding

Page 15: Renal Pathophysiology

Urinary Tract Infection (UTI)

• Acute cystitis

– Cystitis is an inflammation of the bladder– Most common pathogen: E. coli

Page 16: Renal Pathophysiology

Cystitis• Clinical Manifestations

– Small % asymptomatic– Frequency, urgency, dysuria, hematuria, lower

abdominal or suprapubic pain

• Diagnostic Testing– Urinalysis

• Dipstick– WBC (Pyuria) , RBC, Nitrites– Pink/Cloudy May culture urine

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Page 17: Renal Pathophysiology

Acute Pyelonephritis

• Infection of the renal pelvis and interstitium• Etiology

– Ascending bladder infection– Indwelling urinary catheters– Post cystoscopy– Prostate enlargement– Renal Stones– Reflux– Genetic

17

Page 18: Renal Pathophysiology

Acute Pyelonephritis• Pathogenesis

– Development of infection

– WBC infiltration and inflammation of renal parenchyma

– Altered renal function

– Recurrent infections may lead to scarring and chronic kidney disease

18

Page 19: Renal Pathophysiology

Acute Pyelonephritis

• Clinical Manifestations– Usually, sudden onset– Bacteriuria, fever, flank pain, chills, dysuria, WBC casts in urine

• Complications– Risk of permanent decrease in kidney function

is low– Renal damage from repeated

infections/chronic pyelonephritis19

Page 20: Renal Pathophysiology

Chronic Pyelonephritis

• Etiology– Recurrent and/or improperly treated infections– Obstructive disorders– Vesicoureteral reflux

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Page 21: Renal Pathophysiology

Chronic Pyelonephritis

• Pathogenesis

– Repeated invasion of leukocytes and subsequent inflammation of renal parenchyma with recurrent infection

– Fibrosis and scarring of renal tubules decreases the number of functioning nephrons

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Page 22: Renal Pathophysiology

Chronic Pyelonephritis

• Clinical Manifestations

– Similar to acute• Found during routine evaluation for other conditions

– Azotemia

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Page 23: Renal Pathophysiology

Glomerular Abnormalities

23

Glomeruli are part of the nephron.

Fluid filtration from the blood to the nephron tubules takes placein the glomeruli.

Average GFR is 125 ml/min.

Nephron

Page 24: Renal Pathophysiology

Glomerular Disorders

• Glomerulonephritis– Inflammation of the glomerulus

• Immunologic abnormalities (most common)• Drugs or toxins• Vascular disorders• Systemic diseases• Viral causes

– Most common cause of end-stage renal failure

Page 25: Renal Pathophysiology

Glomerulonephritis

• Clinical Manifestations– Hematuria

– Red cell casts

– Proteinuria

– Signs of fluid retention due to GFR

25

Page 26: Renal Pathophysiology

Nephrotic Syndrome

• Excretion of 3.5 g or more of protein in the urine per day

• The protein excretion is caused by glomerular injury

• Findings– Hypoalbuminemia, edema, hyperlipidemia,

and lipiduria, and vitamin D deficiency

Page 27: Renal Pathophysiology

Acute Renal Failure

• Etiology– Decreased perfusion– Pyelonephritis– Drug toxicity– Autoimmune disease/glomerulonephritis– Contrast induced nephropathy

27

Page 28: Renal Pathophysiology

Acute Renal Failure

• Classification– Pre-renal

– Post-renal

– Intra-renal

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Page 29: Renal Pathophysiology

Acute Renal Failure

• Clinical Manifestations– Sudden and near complete cessation of renal

function• Oliguria• Anuria• FVE, HTN• Elevated BUN, Creatinine• Fluid & Electrolyte imbalance

– Changes in LOC– Cardiac dysrhythmias

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Page 30: Renal Pathophysiology

Chronic Renal Failure• Defined as decrease in kidney function or

kidney damage for 3 months or longer.

• Progressive loss of renal function– Tubular atrophy, glomerulosclerosis, interstitial

fibrosis– Damage to nephrons– Irreversible; terminates in ESRD

30

Page 31: Renal Pathophysiology

Chronic Renal Failure

• Etiology/Risk Factors– Diabetes Mellitus

– Glomerulonephritis

– HTN

– Cystic Kidney Disease

– Other

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Page 32: Renal Pathophysiology

Chronic Renal Failure• Stages-based on degree of nephron loss and

clinical manifestations– Decreased Renal Reserve <75% nephron loss,

no s/s– Renal Insufficiency 75-90% nephron loss,

polyuria, nocturia, slight increase in BUN and creatinine, maybe controlled by diet and meds

– End Stage Renal Disease (ESRD) > 90% nephron loss, azotemia/uremia, F&E problems, anemia, dialysis or transplantation necessary

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Page 33: Renal Pathophysiology

Chronic Renal Failure

• Clinical Manifestations of ESRD

– Increased BUN 180 – 200 mg/dL

– FVE decreased GFR and activation of RAAS

– Electrolyte imbalance- retention of K, Mg, Phos

– Uremic Syndrome -confusion, anorexia, N/V, pruritis,

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Page 34: Renal Pathophysiology

Chronic Renal Failure

• Alterations seen in following systems:

– Musculoskeletal

– Cardiovascular and pulmonary

– Hematologic

– Immune

Page 35: Renal Pathophysiology

Chronic Renal Failure

– Neurologic

– Gastrointestinal

– Endocrine and reproduction

– Integumentary