Module 8: Renal System Flashcards by LENNIE BELLE PORTENTO

Formation of Kidney stones

Nephrolithiasis

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Formation of stones in the Urinary tract

Urolithiasis

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Formation of stones in the “Duct”

Lithiasis

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Account for 80% of all stones
Small, hard Stones (1-3mm)
Stones have sharp edges
Radio-Opaque

Calcium Stones

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Large Stones (Molds to Renal Pelvis/Calyces) ʹ Hence Staghorn͘
Chronic Irritation of Epithelium surrounding
Stone > Squamous Metaplasia

Triple Phosphate/Struvite/ “Staghorn” Stones

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Clinical Features:
- Usually, Unilateral o Painful Hematuria ʹ
Macro/Micro
- Writhing in pain͕ pacing about and unable
to lie still͟
- Hydronephrosis > Stretching of Renal
Capsule > Flank Pain & Tenderness.

Lithiasis (Clinical features of Lithiasis)

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Deep flank pain. No radiation.
Distension of the Renal Capsule

Stone in Ureteropelvic Junction

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Intense, Colicky
Pain (Loin > Inguinal Region >
Testes/Vulva) + N/V

Stone in Ureter

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Dysuria, Frequency, + Tip of penis
pain

Stone in Ureterovesical Junction

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Management: Daily Na-Bicarbonate, (ESWL) Extracorporeal Shock-Wave Lithotripsy, Surgical

Lithiasis (Management of Lithiasis)

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What Location?
- may cause flank discomfort, recurrent
infection or persistent hematuria
- may remain asymptomatic for years and
not require treatment

calyx

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What Location?
- tend to cause UPJ obstruction renal pelvis
and one or more calyces

pelvis

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What Location?
- often associated with infection
- infection will not resolve until stone
cleared

staghorn calculi

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What Location?
- 5 mm diameter will pass spontaneously in
75% of patients the three narrowest
passage points for upper tract stones
include: UPJ, pelvic brim, UVJ

ureter

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Factors promoting stone formation?

(INC Ca, Uric, Oxalate) CUO
hypercalciuria
increased oxalate
increased uric acid

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Ca2+ oxalate most common, followed by
Ca2+ phosphate description
- grey or brown due to hemosiderin from
bleeding
- radiopaque

Calcium Stones

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Female patients affected twice as often as
male patients
- account for 10% of all stones
- contribute to formation of staghorn
calculi
- consist of triple phosphate (calcium,
magnesium, ammonium)

Struvite Stones

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Account for 10% of all stones
- orange colored gravel, needle
shaped crystals
- radiolucent on x-ray
- filling defect on IVP
- Radiopaque on CT scan
- Visualized with ultrasound

Uric Acid Stones

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Autosomal recessive defect in small bowel
mucosal absorption and renal tubular
absorption of dibasic amino acids
- Seen in children and young adults
- Aggressive stone disease

Cystine Stones

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hexagonal on urinalysis
o yellow, hard
o radiopaque (ground glass)
o staghorn or multiple
o decreased reabsorption of “COLA”

Cystine Stones

COMMON INFECTIONS OF THE URINARY
SYSTEM: Infection of the renal parenchyma with local and systemic manifestations of infection
- may be classified as uncomplicated or
complicated

Acute Pyelonephritis

Usually ascending microorganisms, most
often bacteria. causative microorganisms are usually E. coli, Klebsiella, Proteus, Serratia, Pseudomonas, Enterococcus, and S. aureus

Acute Pyelonephritis

Laboratory Investigations of Pyelonephritis?

Urine dipstick, Microscopy, Gram negative rods, Gram positive cocci, Culture: > 105 colony forming units

Type of Acute Pyelonephritis: in the absence of
conditions predisposing to anatomic
or functional impairment of urine
flow

uncomplicated

Type of Acute Pyelonephritis: occurring in the setting of renal or ureteric stones, structures, prostatic obstruction (hypertrophy or malignancy), vesicoureteral reflux, neurogenic bladder, catheters, DM, sickle-cell hemoglobinopathies, polycystic kidney disease, immunosuppression, and post-renal transplant

complicated

Treatment of Pyelonephritis

TMP/SMX, fluoroquinolone, third generation cephalosporin, start broad spectrum IV antibiotics

A form of chronic tubulointerstitial nephritis of bacterial origin - Cortical scarring, tubulointerstitial damage, and calyceal deformities seen

Chronic Pyelonephritis

Characterized by significant proteinuria, hypoalbuminemia, edema, and hyperlipidemia, Normal GFR

Nephrotic syndrome

Characterized by hematuria, proteinuria, and variable degrees of decreased glomerular filtration rate (GFR)

Nephritic syndrome

THE Childhood cause of Nephrotic Syndrome (1-8yrs) Etiology: - Post-Infective (URTI)

MCD (Minimal Change Disease) / Foot Process Disease/ Nil Disease)

>50% of Adult Nephrotic Syndrome: Etiology - Autoimmune - Ag : Ab Complex Deposition

MGN (Membranous Glomerulonephrosis)

<35% of Adult Nephrotic Syndrome - Vey similar to MCD but in adults Etiology: Same as MCD - Often a recent history of an URTI - Nephrotic Syndrome - +++ Selective Proteinuria - Prognosis – Poor: 30% Remission; 50% CKD and 20% RPGN

FSGS (Focal Segmental Glomerulosclerosis)

THE Childhood cause of Nephritic Syndrome (3-15yrs). Post-Infective (GABH-Streptococcal Pharyngitis) Ag:Ab Complex Deposition

PSGN (Post-Strep Glomerulonephritis)

IgA-Nephropathy = THE Adult (15-30yrs) Cause of Nephritic Syndrome. -Autoimmune - Ag:IgA Complex Deposition in Glomerulus - 30% > Slowly Progressive - 10% > Renal Failure

IgA Nephropathy (Berger’s Disease)

NOT a Separate Disease; ANY Glomerulonephritis can > RPGN Etiology: - Progression of any Glomerulonephritis (Autoimmune) - Rapidly Progressing Glomerulonephritis > Renal Failure within Weeks - Poor: Quickly progresses to ESRF (end stage renal failure)

RPGN (Rapidly Progressive Glomerulonephritis)

Rapid loss of kidney function Clinical features: Uremia, Hyperkalemia, Fluid Retention, Hematuria, Flank pain

Acute Renal Failures

Before the Blood Reaches the Kidney (Ie. Dec. Glomerular Perfusion) o Hypovolemia (Eg. Blood Loss) o Decreased cardiac output (Eg. Heart Failure) o Renal artery obstruction (Eg. Embolism)

Pre-Renal Failure

The kidney itself is damaged - Acute glomerular nephritis - Tubular diseases e.g., acute tubular necrosis - Interstitial diseases e.g., auto immune disorders such as SLE - Vascular diseases e.g., polyarteritis nodosa

Intra-Renal Failure

Due to outflow obstruction from the kidneys o Cancer - Bladder / Prostate / Ureteric / Cervical o Blood clot o Calculi (Kidney stones - Bilateral) o Accidental surgical ligation

Post-Renal Failure

What Stage of Chronic Renal Failure? > 90 ml/min GFR (Normal) plus other signs of renal disease

Stage 1

What Stage of Chronic Renal Failure? 90-60 ml/min GFR

Stage 2

What Stage of Chronic Renal Failure? 60-30 ml/min GFR

Stage 3

What Stage of Chronic Renal Failure? 30-15 ml/min GFR

Stage 4

What Stage of Chronic Renal Failure? <15 ml/min GFR

Stage 5

DEC Blood Urea: Creatinine Ratio (Infection/toxin/Ischemia/Hypoxia)

Intra Renal Failure

INC Blood Urea: Creatinine Ratio

Pre Renal (Hypotension/ Dehydration /Normal Kidney) OR Post Renal (BPH/Bladder Stone/Normal Kidney)

- Continuum of progressive nephron loss and declining renal function - Asymptomatic until severe insufficiency develops -Frequently patients present at end-stage with small, contracted kidneys, unknown etiology

Chronic Renal Failure

Types of classifications of Chronic Renal failures are...

glomerular, tubulointerstitial disease, vascular, hereditary