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Renal Disease Ricki Otten MT(ASCP)SC [email protected]

Renal Disease Ricki Otten MT(ASCP)SC [email protected]

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Page 1: Renal Disease Ricki Otten MT(ASCP)SC uotten@unmc.edu

Renal Disease

Ricki Otten MT(ASCP)SC

[email protected]

Page 2: Renal Disease Ricki Otten MT(ASCP)SC uotten@unmc.edu

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Review the Objectives

• Those objectives marked with ‘*’ will not be tested over during the Student Lab Rotation

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Classification of Renal Disease

Usually by specific structural component

affected by disease

1. Glomerular Disease

2. Tubular Disease

3. Interstitial Tissue Disease

4. Vascular Disease

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Glomerular Disease• Most often due to damage to glomerular

basement membrane– Immunologic disease– Metabolic disease– Hereditary disease

• Basement membrane damage leads to– Morphologic changes – Altered glomerular function– Increased permeability allowing leakage of

cells and protein into urine

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Glomerular Disease• Classification

– Primary: specifically affects the kidney• Acute glomerulonephritis• Chronic glomerulonephritis• Nephrotic syndrome

– Secondary: another disease process affects the health of the glomerulus

• Systemic disease (diabetes mellitus, SLE) • Hereditary disorder

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Glomerular Injury

• Clinical features dependent upon– Number of glomeruli involved– Mechanism of injury– Rapidity of disease onset

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Glomerular Injury• Clinical findings:

– Urinalysis: proteinuria, hematuria

– Oliguria

– Physical findings: edema, hypertension

– Blood evaluation: hypoproteinemia, azotemia

(increased urea, creatinine)

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Glomerular Disease

• Acute glomerulonephritis

• Chronic glomerulonephritis

• Nephrotic syndrome

• Diabetes mellitus (nephropathy)

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Acute Glomerulonephritis• Acute post-streptococcal glomerulonephritis

– Relatively common, often in children, also adults– Occurs 1-2 weeks post streptococcal infection– Antibody mediated: blood cultures negative

• Clinical findings:– Sudden onset, fever, malaise, nausea– Oliguria– Edema (lower extremities (ankles), eyes)– Mild hypertension

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Acute Glomerulonephritis• Urinalysis

– Physical Color? Clear?– Chemical– Microscopic

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Acute Glomerulonephritis• Urinalysis

– Physical yellow, hazy– Chemical ?– Microscopic

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Acute Glomerulonephritis• Urinalysis

– Physical yellow, hazy

– Chemical + Blood

Proteinuria (mild)

(<1.0 gram/24 hour)

– Microscopic: ?

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Acute Glomerulonephritis• Urinalysis

– Microscopic:

RBC (some dysmorphic)

WBC

RTE

Casts: RBC hemoglobin granular

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Acute Glomerulonephritis• Other testing:

– Blood• ASO titer• Decreased complement (Antigen-Antibody mediated)• Increased BUN, increased creatinine• Decreased albumin

– Urine• Decreased CrCl = Decreased GFR• Proteinuria (mild: <1.0 grams/24 hr)

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Acute Glomerulonephritis• Majority (>95%) of children recover

• Approx 60% of adults recover

• Only 1-2 % post-strep acute glomerulonephritis develop chronic glomerulonephritis

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Chronic Glomerulonephritis• Numerous glomerular diseases develop

chronic glomerulonephritis

• Onset is slow and insiduous taking many years to develop clinical signs and symptoms

• If not treated, may result in death (uremia)

• Clinical findings: same as acute, but worse

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Chronic Glomerulonephritis

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Chronic Glomerulonephritis

• Urinalysis– Physical yellow, hazy– Chemical ?– Microscopic

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Chronic Glomerulonephritis

• Urinalysis– Physical yellow, hazy

– Chemical+ BloodProteinuria (mild-moderate)

(>2.5 and < 3.5 grams/24 hr)Specific gravity: low and fixed

(isosthenuric)

– Microscopic: ?

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Chronic Glomerulonephritis• Urinalysis

– Microscopic

RBC

WBC

RTE

Casts (RBC, hemoglobin, granular, waxy)

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Chronic Glomerulonephritis

• Other testing: – Blood:

• Increased BUN, increased creatinine• Decreased albumin, decreased TSP

– Urine: • Decreased CrCl = decreased GFR• Proteinuria (moderate: >2.5 grams/24 hr)

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Nephrotic Syndrome

• Selective filtering capability of glomerulus is lost

• Many conditions may lead to NS

• Clinical findings: ‘pitting edema’, azotemia, hypertension, oliguria

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Nephrotic Syndrome

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Nephrotic Syndrome

• Urinalysis– Physical yellow, hazy (cloudy ?)– Chemical ?– Microscopic

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Nephrotic Syndrome

• Urinalysis– Physical: yellow, hazy (cloudy ?)

– Chemical: + Blood

Proteinuria (severe)

(>3.5 grams/24 hour)

– Microscopic: ?

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Nephrotic Syndrome

• Urinalysis– Microscopic

RBC

WBC

RTE

Oval Fat Bodies (OFB)

Free fat droplets

Casts (granular, fatty, waxy, RTE)

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Nephrotic Syndrome

• Other testing:– Blood:

• hypoproteinemia (decr albumin, decr TSP)• Increased lipids• Increased sodium

– Urine: • Decreased CrCl = decreased GFR• Proteinuria (severe: > 3.5 grams/24 hr)

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Diabetes Mellitus (Nephropathy)

• Disorder of carbohydrate metabolism

• Renal disease is a major cause of death in the diabetic patient

• Diabetes is leading cause of– Blindness– End-stage renal disease– Limb amputations

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Diabetes Mellitus (Nephropathy)

• Clinical findings:– Polyuria– Polydipsia– Nocturia

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Diabetes Mellitus (Nephropathy)

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Diabetes Mellitus (Nephropathy)

• Urinalysis– Physical Yellow, hazy– Chemical ?– Microscopic

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Diabetes Mellitus (Nephropathy)

• Urinalysis– Physical Yellow, hazy– Chemical

+ Glucose

Proteinuria (mild-moderate)

– Microscopic ?

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Diabetes Mellitus (Nephropathy)

• Urinalysis– Microscopic

RBC

Casts

Yeast, possibly

Depends on extent of renal involvement (disease)

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Diabetes Mellitus (Nephropathy)

• Other testing:– Blood

• Increased glucose• Increased ketones (diabetes mellitus, type 1)

– Urine• Proteinuria: leads to chronic renal failure and death

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Tubular Disease

• Altered tubular function

• Necrosis of tubular epithelium

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Altered Tubular Function

• Caused by– Reabsorption-secretion capability lost– Concentrating-diluting capability lost

• Results in– Build up of waste products in bloodstream– Loss of essential substances into urine

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Altered Tubular Function

• Renal glycosuria– Glucose in urine, renal threshold not exceeded

• Cystinuria

• Cystinosis

• Renal tubular acidosis– Tubules unable to secrete adequate H+ despite

systemic acidosis

Inherited disorders

Cystine crystals in urine

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Urinalysis Findings

• Renal glycosuria: + glucose

• Cystinuria, cystinosis: cystine crystals

• Renal tubular acidosis: pH not as acid as is needed to compensate for systemic acidosis

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Necrosis of Tubular Epithelium

• Destruction of tubular epithelial cells– Toxin– Ischemic event

• Most common cause of renal failure

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Necrosis of Tubular Epithelium

• Clinical presentation: 3 phases– Onset– Renal failure

• Azotemia• Hyperkalemia• Metabolic acidosis• Oliguria

– Recovery

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Acute Tubular Necrosis• Toxic ATN

– Drugs: AminoglycosidesAnestheticsRadiographic dyesChemotherapyAnti-rejection drugs

– Toxins: MercuryLeadCadmiumEthylene glycolPesticidesMushrooms

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Acute Tubular Necrosis

• Ischemic ATN: decreased perfusion of kidneys as a result of hypotensive events

– Sepsis: bacterial infection of bloodstream– Shock– Trauma

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Acute Tubular Necrosis• Urinalysis

– Physical: Yellow, hazy

– Chemical:

Proteinuria (mild), +blood, low specific gravity

– Microscopic:

RBC, WBC, RTE

Casts: RTE, granular, waxy, broad

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Interstitial Tissue Disease

• Lower urinary tract infection– Cystitis (bladder)– Urethritis (urethra)

• Acute pyelonephritis (upper UTI)

• Yeast infection

• Any bacterial or fungal agent can cause a UTI

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Lower UTI

• ~85% of lower UTI caused by

gram-negative rods (fecal E.coli)

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Lower UTI

• Urinalysis– Physical yellow, hazy (cloudy, turbid)– Chemical ?– Microscopic

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Lower UTI

• Urinalysis– Physical yellow, hazy (cloudy, turbid)– Chemical + protein (<0.5 grams/24 hr)

+ leukocyte esterase

+ nitrite

+ blood

– Microscopic ?

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Lower UTI

– Microscopic

WBC

Bacteria

RBC

Transitional epithelial cells (cystitis)

Absence of casts: why?

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Acute Pyelonephritis

• Most common upper UTI

• Two mechanisms causing infection– Bacterial moving from lower to upper urinary

tract– Septicemia localizing in the kidneys

• Incomplete voiding due to obstruction or dysfunction or anatomic abnormality

• Catheterization, pregnancy, diabetes

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Acute Pyelonephritis

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Acute Pyelonephritis

• Urinalysis– Physical Yellow, hazy (cloudy, turbid)– Chemical ?– Microscopic

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Acute Pyelonephritis

• Urinalysis– Physical Yellow, hazy (cloudy, turbid)– Chemical + protein (<1.0 gram/24 hr)

+ leukocyte esterase (WBC)+ nitrite+ bloodspecific gravity: normal to

low

– Microscopic ?

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Acute Pyelonephritis

– Microscopic

WBC (may see clumping)

Bacteria

RBC

RTE

Casts: WBC, granular, RTE, waxy

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Yeast Infection

• Urinary tract of both men and women are susceptible to yeast infection

• Most often vaginal yeast infection contaminates urine

• Often caused by Candida species

(candida albicans)

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Yeast Infection

• Candida species (candida albicans)– Normal flora of GI tract and vagina– Normal bacterial flora keep yeast proliferation

under control– Catheters provide mode of inoculation

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Yeast Infection

• Urinalysis– Physical Color? Clear?– Chemical– Microscopic

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Yeast Infection

• Urinalysis– Physical Yellow, hazy (cloudy)– Chemical ?– Microscopic

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Yeast Infection• Urinalysis

– Physical Yellow, hazy (cloudy)– Chemical + WBC ?

+ blood ?

– Microscopic

Yeast

Mycelial elements

RBC? WBC?

Casts? Why or why not?

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Vascular Disease

• Any disorder that affects the blood flow to the kidneys can cause renal disease

– Cardiac disease (25% of cardiac output)– Atherosclerosis– Hypertension– Diabetes– Eclampsia– Etc

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