UA Renal Diseases

Poststreptococcal glomerulonephritis

Glomerular Disorder

rapidly progressive glomerulonephritis

Glomerular disorder

Good Pasture’s Syndrome

Glomerular disorder

chronic glomerulonephritis

Glomerular disorder

Acute tubular necrosis

Tubular disorder

Fanconi’s syndrome

Tubular disorder

Cystinosis/Cystinuria

Fanconi’s syndrome

Hartnup disease

Fanconi’s syndrome

What kind of crystals does cystinosis and cystinuria present with?

Cystine crystals

Cystitis

Interstitial disorder

Acute pyelonephritis

Interstitial disorder

Chronic pyelonephritis

Interstitial disorder

Acute interstitial nephritis

Interstitial disorder

Most common cause of Cystitis

Lower UTI: bladder infection

Most common cause pyelonephritis

Ascending movement of bacteria from a lower UTI

What does a sudden decrease in GFR, azotemia, and oliguria → anuria indicate

Acute renal failure

Pre-renal (25%) Mechanism

decrease in blood flow below 80 mmHg

Decreased cardiac output, blood loss, sever diarrhea, and vomiting

Renal (65%) Mechanism

damage to the glomerulus or tubular regions

99% present with acute tubular necrosis

Post-renal (10%)

obstructions in urine flow

Crystalline deposition (calculi), neoplasms

Supersaturation of chemical salts in urine

Factor that promotes the formation of kidney stones

Optimal urinary pH usually basic

Factor that promotes the formation of kidney stones

Urinary stasis

Factor that promotes the formation of kidney stones

Nucleation or initial crystal formation

Factor that promotes the formation of kidney stones

75% of renal stones are composed of

Calcium oxalate or calcium phosphate

What causes renal lithiasis

renal calculi form in the calyces and pelvis of the kidney, ureters, and bladder

What is a lithotripsy

use of high energy waves to break stones into smaller pieces

Symptoms of Renal lithiasis

- Pain radiating from the kidney and continuing down to the genitalia and legs

- Nausea and vomiting

- Sweating

- Increased urge to urinate

- Bloody urine

How to manage Renal lithiasis

-maintain urine pH at a level which will prevent crystallization of the crystals in question

-Medications to prevent the excretion of or to change the metabolism of the calculi forming compound

-Adequate hydration to prevent urinary stasis

-Dietary Restrictions

Inulin clearance Advantage

not absorbed by GI system or tubules, not modified, readily passes through glomerulus

Inulin clearance Disadvantages

Exogenous substance that must be administered intravenously during test

Creatinine clearance is not affected by

urine flow rate, not reabsorbed by tubules, and not affected by diet

Creatinine clearance is dependent on

muscle mass

Creatinine clearance is produced at

a constant rate and has a constant serum level

Average production of creatinine is

1.2 mg/day

Beta 2 - Microglobulin mechanism

Dissociates from the membrane of nucleated cells at a constant rate and is rapidly filtered by the glomerulus. Then it is absorbed and catabolized by the tubules.

A rise in serum Beta 2 - Microglobulin is

more sensitive indicator of a decrease in GFR rather than creatinine clearance

when is Beta 2 - microglobulin not reliable

patients with immunologic disorders or with malignancy

Beta 2 - Microglobulin is a good test to assess

tubular function

(serum levels are normal but urine concentration increases)

Cystatin C is readily filtered by

the glomerulus and reabsorbed and broken down by tubules (does not re-enter circulation)

What happens to the serum levels of Cystatin C when GFR decreases

Cystatin C increases

Cystatin C is recommended for

Pediatric patients, elderly, diabetics, and critically ill

Cystatin C is independent of

muscle mass

Cystatin C is produced at a

constant rate by all nucleated cells

Normal GFR

>90 mL/min

GFR when at risk of uremia

60-90 mL/min

GFR when a physician needs to be consulted; uremia

<60 mL/min

GFR when a patient requires dialysis or transplantation; uremia

<30 mL/min

GFR is important for

screening patients for kidney disease

Modification of diet in Renal disease (MDRD) calculation

parameter used in calculating eGFR

Uses serum creatinine, age, gender, and ethnicity to estimate GFR

parameter used in calculating eGFR

Healthy patients reported as >60 mL/min/1.73 m^2

parameter used in calculating eGFR

Hemodialysis is mostly done at

the hospital

Peritoneal Dialysis can be done at

home

What does Hemodialysis do?

Patient’s blood is cleansed as particles diffuse across a semipermeable membrane into a commercially available dialysis solution

-Dialysis solution contains sodium, chloride, and some glucose to prevent their loss from the blood

What is the preferred access point in Hemodialysis

Fistula (a surgical connection between a vein and an artery)

What is the recommended treatment of Hemodialysis

4 hours a day

3 days a week

How does Peritoneal Dialysis work?

-Sterile solution of dialysis solution drains into the peritoneal cavity

-The peritoneal membrane acts as a selectively permeable membrane that allows diffusion and osmosis of wastes into the dialysis solution

-Once in equilibrium, the dialysis solution is drained and discarded

How often does the Peritoneal Dialysis occur

Exchanges 4-5 times per day

Etiology of acute poststreptococccal glomerulonephritis

Occurs in children and young adults following infection with certain strains of group A beta hemolytic streptococcus

Immune complexes deposit on the glomerular membranes

Ensuing inflammation damages glomeruli

Symptoms of acute poststreptococccal glomerulonephritis

Rapid onset of hematuria and edema

Fever, hypertension

Oliguria -> anuria

Lab results of acute poststreptococccal glomerulonephritis

Blood cultures: neg

Antistreptolysin O titer and anti-group A streptococcal enzyme studies will be elevated

Increased serum BUN

UA results of acute poststreptococccal glomerulonephritis

- Marked Hematuria

- Proteinuria

- RBC Casts

- Hyaline Casts

- Granular Casts

- WBCs

Prognosis of acute poststreptococccal glomerulonephritis

Permanent kidney damage seldom occurs

Etiology of rapidly progressive glomerulonephritis

Deposition of immune complexes in glomerulus leading to the formation of crescentic structures in Bowman’s space composed of macrophages, fibrin, and fibroblasts.

Crescentic structures permanently damage the glomerulus and occlude the PCT

Often associated with infections and Systemic Lupus Erythematosus (SLE)

UA of rapidly progressive glomerulonephritis

Hematuria

Low GFR

Proteinuria

Prognosis of rapidly progressive glomerulonephritis

Permanent damage to nephrons (chronic glomerular nephritis) → end stage renal failure

Etiology of Good Pasture’s Syndrome

Anti-glomerular basement membrane autoantibody formed after viral respiratory infection or inhalation of chemicals causing pulmonary injury – complement activation destroys capillaries

Symptoms of Good Pasture’s Syndrome

Hemoptysis (spitting up blood)

dyspnea

UA of Good Pasture’s Syndrome

Proteinuria

hematuria

RBC casts

Prognosis of Good Pasture’s Syndrome

Progression to chronic glomerulonephritis and end-stage renal failure

Etiology of chronic glomerulonephritis

Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders; glomeruli become hyalinized and acellular

Symptoms of chronic glomerulonephritis

Fatigue, anemia, hypertension, edema, markedly decreased GFR, Increased BUN and Creatinine, Electrolyte imbalance

UA of chronic glomerulonephritis

- Hematuria

- Proteinuria

- Glucosuria (with progressive tubular damage)

- RBC and WBC Casts

- Granular Casts

- Waxy and broad casts

Prognosis of chronic glomerulonephritis

Continually will worsen until kidney failure

Etiology of nephrotic syndrome

Glomerular damage coupled with the disruption of the electrical charge of the tubular epithelium results in a leaky tubular epithelium

Minimal change disease: in children

Membranous glomerulonephritis: in adults

Symptom of nephrotic syndrome

Edema

Lab findings of nephrotic syndrome

- Serum hypoproteinemia (albumin)

- Serum hyperlipidemia

- Low immunoglobulins

- Low coagulation factors

- Azotemia

- Hypertension

UA of nephrotic syndrome

- Proteinuria >3.5 g/day

- Hematuria (uncommon in minimal change disease)

- Lipiduria (free floating and oval fat bodies)

- Oliguria

- Fatty casts

- Waxy casts

- Renal tubular cell casts

Prognosis of nephrotic syndrome

Gradual progression to chronic renal failure

Etiology of acute tubular necrosis

Damage to the renal tubular cells caused by

- Ischemia: Shock, cardiac failure, massive hemorrhage,

- Toxic agents

Peripheral Blood lab results of acute tubular necrosis

- Low hemoglobin and hematocrit (shock)

- Elevated cardiac enzymes (heart failure)

UA of acute tubular necrosis

- Hematuria

- Mild proteinuria

- Renal tubular epi cells especially in sheets (RTE)

- Renal tubular epi cell casts

- Hyaline casts, granular casts, waxy casts, and broad casts

Prognosis of acute tubular necrosis

Variable dependent upon underlying cause

Etiology of Fanconi’s syndrome

generalized failure of reabsorption in the PCT

Solutes such as glucose, sodium, potassium, bicarb, phosphorus, and amino acids are not being reabsorbed normally

Inherited or acquired

Fanconi’s syndrome is caused by

Cystinosis/cystinuria, Hartnup, Toxin Exposure, Amyloidosis, Rickets, complications of multiple myeloma or renal transplant

Lab results of Fanconi’s Syndrome

- Abnormal serum electrolytes

- Abnormal amino acid chromatography

- Normal blood glucose

UA of Fanconi’s Syndrome

- Glucose

- Cystine crystals (if cystinosis or cystinuria)

Prognosis of Fanconi’s syndrome

Requires supportive therapy

Etiology of Cystitis

Lower UTI: Bladder infection

Symptoms of Cystitis

Pain and burning during urination

Dysuria

Increased frequency of urination

Mental confusion, agitation, and/or withdrawal in elderly

Lab results of cystitis

- BUN: normal

- Plasma/serum creatinine: normal

- Positive urine culture

UA of Cystitis

- Protein: neg or small

- Nitrite: pos

- Blood:+/-

- Leukocyte esterase: pos

- RBC, HGB, WBC casts: none (below kidney)

- Bacteria: small -> large

Etiology of acute pyelonephritis

Infection of the tubules and interstitium

Caused by: Ascending movement of bacteria from a lower UTI (most common); reflux nephropathies

Symptoms of acute pyelonephritis

Burning during urination

Increased frequency of urination

Flank and lower back pain

Nausea and headache

Confusion, agitation, and/or withdrawal in elderly

Lab results of acute pyelonephritis

- Bacteremia +/-

- Creatinine: Normal to slt increased

- BUN: normal to slt increased

- Urine culture: positive

UA of acute pyelonephritis

- Protein: small

- Blood: +/-

- Nitrite: pos

- Leukocyte esterase: pos

- WBC casts: present

- Bacteria: small to large

Prognosis of acute pyelonephritis

Proper antibiotic treatment should resolve the problem without permanent damage to tubules

Etiology of chronic pyelonephritis

Occurs when persistent inflammation of the renal tissue causes permanent scarring that involves the renal calyces and pelvis

- Accumulation of fibrosis causes renal calyces to be permanently dilated and deformed

- Most common: reflux nephropathies (multiple kidney infections)

Lab results for chronic pyelonephritis

- Blood culture +/-

- BUN: Increased

- Urine culture: pos

- Hypertension

- Polyuria

UA of chronic pyelonephritis

- Leukocyte esterase pos

- Nitrite pos

- Blood present

- Protein present

- Bacteria Pos

- WBC casts: present

- Bacterial casts: present – rarely seen

- Granular and waxy broad casts: present

- Low specific gravity