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HCR240-Chapter22RenalDisorders.pptx

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Chapter 22

Renal Disorders

Kidneys

Organs of filtration and secretion

Also play a role in:

Acid/base balance, blood pressure regulation

RBC formation, drug metabolism

Hormone metabolism, vitamin D synthesis

Glucose homeostasis

Alterations in kidney function can impair all of these processes

Kidneys (continued)

Incidence of kidney disease growing in U.S.

Diabetes mellitus, hypertension, autoimmune conditions play a role

End-stage renal disease (ESRD) has significantly increased

Basic Concepts Renal Function

Kidneys receive ~1/5 of cardiac output

Glomerular filtration rate (GFR)

Renal blood filtered per unit of time

Directly related to renal perfusion

Decrease renal perfusion = decrease GFR

GFR reduction with aging

Nephron and Excretory Function

Nephron

Basic functional unit of kidney

Processes filtered fluid

End product: urine

Glomerular capillaries

Specialized capillaries

High hydrostatic pressure favors filtration

Filtrate moves into Bowman’s capsule (initial portion of nephron)

Nephron Overview

Proximal tubule

Segment following Bowman’s capsule

Reabsorbs majority of filtrate

Loop of Henle

Begins to concentrate filtered fluid

Urea: a waste product enters Loop of Henle

Distal tubule

Under influence of aldosterone, absorbs water and sodium

Collecting ducts

Under influence of ADH, additional water reabsorbed

Nephron

Kidney Functions

Acid-base balance

Excrete/reabsorb H+ ion and bicarbonate as needed

Waste elimination

Urea, uric acid, creatinine (Cr), drug metabolites

Secretory function

Erythropoietin (EPO)

Increase RBC’s in response to hypoxia

Renin

Released in response to low BP or perfusion

Activate RAAS (renin-angiotensin-aldosterone)

Kidney Functions (continued)

Vitamin D synthesis and calcium balance

Kidney activates vitamin D

Vitamin D important in calcium absorption

Glucose homeostasis

Renal threshold to reabsorb glucose (BG of 180 mg/dL)

If exceeded, glucose appears in urine

Kidneys degrade insulin

Gluconeogenesis

Kidney Dysfunction Consequences

Insufficient filtration

Waste product buildup

Urine not concentrated

Toxin buildup leading to destruction of blood cells

Neurological

Confusion, stupor, encephalopathy

Excess renin secreted, raising BP

Decreased erythropoietin, decreasing RBC’s

Acid-base balance not maintained

Excess K+ not secreted

Decreased vitamin D; decreased Ca++ absorption (renal osteodystrophy)

Basic Pathophysiology

Kidneys susceptible to ischemic injury

High pressure required to push fluid through kidneys and urinary system

Nephrons can be harmed by toxins

Urine outflow must be maintained

Uropathy

Obstruction of urine flow

Can cause fluid backup which damages renal pelvis

Categories of Renal Dysfunction

Prerenal

Decreased blood flow and perfusion to the kidney

Intrarenal

Actual injuries to the kidney

Postrenal

Obstruction of urine outflow from the kidneys

Renal Dysfunction

Prerenal Dysfunction

Any condition that directly or indirectly decreases renal perfusion

Hypovolemia, heart failure, shock

Injury results from ischemia

Sufficient blood pressure also needed to maintain glomerular filtration and urine output

Intrarenal Dysfunction

Direct damage to kidney

Trauma to kidney

Pyelonephritis, autoimmune conditions (lupus)

Infection of kidney

Post-streptococcal glomerulonephritis

Nephrotoxic drugs

NSAID’s, ACE inhibitors, angiotensin-receptor blockers, statins, some antibiotics

Postrenal Dysfunction

Obstructive uropathy

Prevents urine outflow from the kidney

Hydronephrosis

Urine back up into kidney

Examples:

Kidney stone

Prostate gland hyperplasia

Acute Tubular Necrosis (ATN)

Ischemia and hypoxia damage to nephron

Ischemia causes sloughing of nephron tubule cells into nephron lumen

Lumen becomes blocked, preventing fluid flow and urine formation

Common cause of acute kidney injury (AKI)

May lead to renal failure

Costovertebral Angle (CVA)

Acute Glomerulonephritis (AGN)

Immunological mechanism

Triggers inflammation that damages the membranes of the glomerulus

Autoimmune or post-streptococcal disorder

PGSN: post-streptococcal glomerulonephritis

Can progress to ESRD

Antigen-antibody reaction damages glomeruli leading to hyperpermeability

Acute Glomerulonephritis (AGN) (continued_1)

Damaged glomeruli leads to:

Protein loss

Edema (periorbital)

Oliguria

Hypervolemia (HTN)

PGSN: 7 to 21 days post- strep infection

Dark urine: RBC’s

Acute Glomerulonephritis (AGN) (continued_2)

Diagnosis

Elevated serum Cr and BUN; low serum albumin

Urinalysis: protein, WBC’s, blood

Antibodies to streptococcal bacteria may be present

Treatment

Antibiotics, dietary modifications, diuretics

Nephrotic Syndrome

Glomerular damage resulting in proteinuria and edema

Most commonly caused by diabetes mellitus, amyloidosis, and lupus

Massive albuminuria (with facial edema), hematuria, HTN, oliguria

Hyperlipidemia may develop

Lipid synthesis by liver increases, as liver increases albumin synthesis to compensate for urinary loss

Treatment

Adequate fluid, dietary modification, may progress to renal failure

Proteinuria

Nephrolithiasis

Stones (calculi) in kidneys

Urolithiasis

Stone travels to ureter

Presentation based on stone’s location

Stones

Calcium (most common), struvite, uric acid, cystine

Kidneys secrete stone-inhibitors

Risk Factors for Nephrolithiasis

Genetic susceptibility

Dehydration

Hypercalcemia

Excessive calcium intake

Hyperparathyroidism

Gout

Hyperuricemia

Urinary tract infection

Immobility

Symptoms of Nephrolithiasis

Severe abdominal, flank pain

Colicky pain caused by ureter spasms

Hematuria

Crystalluria

Hydronephrosis may develop

Diagnosis requires stone analysis

Treatment of Nephrolithiasis

Pain relief

Prevent recurrence and UTI

Strain urine to catch stone for analysis

High fluid intake: greater than 3 liters/day

Lithotripsy

Surgery, if no relief

Dietary changes to keep urine acidic or alkaline, depending on stone composition

Pyelonephritis

Infection of renal pelvis

Ascending UTI

Stasis of urine plays a role

Other factors

Obstructive uropathy

Vesicoureteral reflux

Anatomical abnormality (urine refluxes from bladder into ureters)

Neurogenic bladder

Urological instrumentation

Pregnancy

Pyelonephritis Signs and Symptoms

Fever (uncommon in lower UTI)

Abdominal or CVA tenderness

Flank pain

Nausea and vomiting

Chills

Dysuria

Urinary frequency

Microscopic hematuria

Pyuria (WBC’s in urine)

+Leukocyte esterase test of urine

Diagnosis of Pyelonephritis

Urine cultures

E. coli (most common cause), S. saprophyticus, P. mirabilis

Dipstick urinalysis

Pyuria, positive leukocyte esterase

Contrast-enhanced helical/spiral computed tomography (CECT)

CT scan

Kidney, ureters, bladder (KUB)

Ultrasound

Treatment of Pyelonephritis

Antibiotics

Analgesics, if needed

Fluid intake greater than 3 L/day

Remove urological obstruction, if present

Chronic Renal Failure (CRF)

Irreversible and progressive, with gradual onset

90% to 95% of the nephrons affected

Usually progresses to ESRD

Hemodialysis or kidney transplant needed

DM, HTN, glomerulonephritis, and PKD are leading causes

Five Stages of the Progression of CRF

Stage 1

Kidney damage with normal or increased GFR (greater than 90 mL/min)

Stage 2

Mild reduction in GFR (60 to 89 mL/min)

Stage 3

Moderate reduction in GFR (30 to 59 mL/min)

Symptoms normally become apparent

Serum Cr and BUN increase

Stage 4

Severe reduction in GFR (15 to 29 mL/min)

Stage 5

Kidney failure (GFR lower than 15 mL/min)

Complications of CRF

Uremic encephalopathy

Proteinuria

Hypoalbuminemia

Edema

Fluid overload

Oliguria

Electrolyte imbalances

Hemolysis

Thrombocytopenia

Anemia

Decreased vitamin D

Hypertension

Metabolic acidosis

Hyperkalemia

Hypocalcemia

Hyperphosphatemia

Hyperparathyroidism

(due to Ca++ loss, leads to renal osteodystrophy)

CRF

Diagnosis

CBC, BUN, and Cr serum levels, urinalysis, albumin levels

Renal imagining studies

Treatment

Fluid and electrolyte management, along with BP management

GFR less than 10–20 mL/min—dialysis, kidney transplant evaluation

MODULE 7

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