Nurs 245 Ch 33 - Disorders of Renal Function

Urinary System

contains 2 kidneys, 2 ureters, 1 bladder, and 1 urethra

• maintains homeostasis by managing the volume and composition of fluid reservoirs, primarily blood

Kidneys

bean-shaped organs located at the back of the abdominal cavity - retroperitoneal

Ureters

thin muscular tubes that connect each kidney to the urinary bladder

urinary bladder

strong, muscular organ that is responsible for storage and elimination of urine

urethra

a tube that carries urine from the bladder to the outside of the body

Renal capsule

thin over covering of the kidney

renal cortex

the outer region of the kidney that contains renal corpuscles and parts of the renal tubules

renal medulla

inner region of the kidney

• contains the renal pyramids

renal calyces

cup-shaped structures that collect urine from the renal pyramids

Renal pelvis

funnel-shaped cavity inside the kidney

• connects the urine from renal calyces

• continues and becomes ureters

Neprhon

the structural and functional unit of the kidney and produces urine through three main processes

• glomerular filtration

• tubular reabsorption

• tubular secretion

Glomerular filtration

movement of protein-free plasma across the glomerular membrane driven by hydrostatic pressure

• main driving pressure is hydrostatic pressure (pushes out urine)

Tubular Reabsorption

movement of fluid and solutes from tubular lumen to the peritbular capillaries

Tubular secretion

transfer of substances from the peritubular capillaries to the tubular lumen

Where does reabsorption occur?

• ascending tract → only solutes (impermeable to water)

• descending tract → only water moves here (impermeable solutes)

• PCT → most reabsorption occurs here

Collecting ducts

where ADH, ADI, and PTH work

Glomerular Filtration Steps

1. glomerular blood hydrostatic pressure is the highest force (pushing fluid outwards)

2. capsular hydrostatic pressure (inward force, the lowest force)

3. blood colloid osmotic pressure (inward force)

Afferent Arteriole and Efferent Arterioles

Afferent → brings blood to the glomerulus and has a larger diameter (more blood entering than leaving)

Efferent → brings blood away from glomerulus

Large cells and proteins

cannot be filtered (protein should not be in the urine)

GFR

volume of fluid that is filtered from the blood by both kidneys per minute

• healthy adults have a GFR of approx. 120-125 mL/minute

Autoregulation

the kidneys maintain a relatively constant GFR despite changes in systemic BP

• two main mechanisms are the myogenic mechanism and tubuloglomerular feedback

Myogenic mechanism

when arterial BP increases, the afferent arteriole stretches

the smooth muscle in the arteriole contracts (vasoconstriction)

limits blood flow into the glomerulus (GFR decreases)

• myogenic mechanism is based on the stretch in afferent arteriole

Tubuloglomerular feedback

the mechanism involves the macula densa cells of the distal tubule, which detect sodium chloride (NaCl) delivery

• when NaCl delivery increases, the macula densa signals the afferent arteriole to constrict (to decrease GFR)

• when NaCl delivery decreases, the afferent arteriole dilates (to increase GFR)

vasoconstriction always causes decreased GFR

vasodilation always causes increased GFR

Hormonal Mechanism

GFR is regulated by several hormones that alter renal blood flow, glomerular capillary pressure, and the diameter of the afferent and efferent arterioles

Angiotensin II

constricts the afferent and efferent arterioles to decrease GFR

Atrial Natriuretic Peptide (ANP)

dilates the afferent arteriole to increase GFR

Frequency of Urgency, Dysuria, Nocturia, and Incontinence

• Frequency and urgency –- sudden, compelling urge to void

  • Frequent need to urinate or feeling a sudden and persistent need to urinate.

• Dysuria –- painful urination

  • Burning or painful sensation during or immediately after urination

• Nocturia – waking up frequently at night to urinate

• Incontinence – involuntary or accidental leakage of urine

manifestations of urinary disorders

Hematuria, Proteinuria, Bacteriuria, Pyuria, Urinary Casts

• Hematuria: visible (gross) or microscopic– (detectable under a microscope) blood in the urine

• Proteinuria: presence of excess protein in the urine –- usually albumin

• Bacteriuria: presence of bacteria in the urine.

• Pyuria –- pus in urine

  • High number of leukocytes in the urine

• Urinary casts: tube-shaped microscopic structures formed in the kidney's renal tubules

  • Presence in the urine confirms the disorder originating in the kidney nephrons

all abnormal findings in urinalysis

Urinalysis

urine testing

Renal Agenesis

congenital condition in which one or both kidneys fail to develop before birth

• common types are unilateral renal agenesis (absence or severe underdevelopment of one kidney) and bilateral renal agenesis (both kidneys are absent)

• congenital disorder

Hypoplasia

failure of one or two kidneys to develop to normal size (after birth)

• congenital disorder

Ectopic Kidney

abnormal position of the kidney

• congenital disorder

• common types: pelvic kidney (kidney remains in the pelvic regions) and crossed ectopic kidney (the kidney is located on the opposite side of the body)

Horseshoe Kidney

fusion of the two kidneys

• lower poles of the kidneys fused forming a U shaped structure

Cystic Diseases

group of disorders characterized by formation of fluid filled sacs (cysts) in the kidneys

Renal Cyst

dilated nephron tubule

• enlarged cyst may cause compression of the renal vessels, degeneration of renal tissue, obstruction of tubular flow

Simple Cyst

small, solitary cysts

• usually harmless and seen in elderly patients receiving dialysis

• asymptomatic and does not require treatment

Medullary Sponge Kidney

rare, benign congenital kidney condition in which the collecting ducts in the medulla become dilated

• this gives the inner part of the kidney a sponge-like appearance

• predisposes the patients to renal calculi and UTIs (because of impaired blood flow)

Adult Polycystic Kidney Disease

autosomal dominant disorder in which the fluid-filled cysts develop in the kidneys

• abnormal gene located on chromosome 16 (can lead to abnormal proliferation)

• no indications in child and young adults; the first manifestation usually around age 40 years

• multiple cysts develop in both kidneys due to abnormality in tubular cell differentiation; the cysts enlarge the kidney and cause (compression and destruction of kidney tissue, chronic renal failure)

Manifestations of Polycystic Kidney Disease

HTN - one of the earliest signs

flank pain - chronic or intermittent pain in the back due to the enlarged kidneys

hematuria - due to rupture of cyst

infected kidney or UTIs

kidney function gradually declines over time

Obstructive disorders

conditions that prevent urine from flowing normally through the urinary tract leading to urine backup, retention, and hydronephrosis

• classified into upper urinary tract obstruction (urine flow is blocked in the kidneys, renal pelvis, or ureters) and lower urinary tract obstruction (urine flow is blocked in bladder and urethra)

Intrinsic Obstruction

kidney stones, cysts

Extrinsic Compression

outside pressure from pregnancy, endometriosis, and prostate hypertrophy (the #1 cause of obstruction)

Hydronephrosis

water in the kidney; urine is unable to drain properly from the kidney into the bladder

• urine backs up in inside the kidney, causing distention of the renal calyces and pelvis

• most damaging effects of urinary obstruction

Urolithiasis

formation or presence of stones (calculi) anywhere in the urinary tract (kidneys, ureters, bladder, or urethra)

• manifestations mainly occur with obstruction of urine flow

Predisposing factors of urolithiasis

excessive amounts of solutes in filtrate

insufficient fluid intake (major factor in calculi formation)

urinary tract infection

high animal protein consumption (red meat diet)

Calcium Stones

oxalate or phosphate

• most common type; develop with high oxalate diet, dehydration, hyperparathyroidism

Struvite

infectious calculi

• common with UTIs caused by urease-producing bacteria

• urease convert urea to ammonia - staghorn calculus may develop over weeks

Uric Acid Stones

common with high purine diet (animal protein) - purine metabolized to urine acid

Manifestation of Urolithiasis

often asymptomatic, but frequent infections may lead to investigation

• urinary urgency

• frequency

• dysuria

renal colic b/c of obstruction of the ureter from a stone

Renal Colic

obstruction of the ureter

• intense spasms of pain in flank area, radiating to the groin area (lasts until obstruction is removed)

• hematuria

• possible nausea and vomiting, cool moist skin, and rapid pulse

Treatment and Prevention of Urolithiasis

• Treatment

  • Small stones will be passed eventually.

  • Lithotripsy (ESWL) –- large stone are crushed to pass with urine flow

  • Drugs may be used to dissolve small stones partially.

  • Surgery

• Prevention

  • Treatment of underlying condition (e.g UTIs)

  • Adjustment of urine pH through dietary modifications

  • Consistent increase in fluid intake

UTIs (+ lower and upper UTIs)

infection in any part of the urinary system, most common in the lower tract

(bladder and urethra).

• Common infections: urine is an excellent growth medium for microorganisms

lower urinary tract infections (cystitis and urethritis) and upper urinary tract infections (pyelitis and pyelonephritis)

Pathogens of UTIs

• Most uncomplicated UTIs caused by Escherichia coli –- bacteria that is normally present in the colon (causes ascending infection)

• Other uropathic pathogens include

  • Staphylococcus saprophyticus in uncomplicated UTIs

• Gram-negative rods (Proteus mirabilis, Klebsiella pneumoniae, Pseudomonas) and gram-positive cocci (Staphylococcus aureus) in complicated UTIs (can become septic infection and septuremia)

• Most UTIs are caused by bacteria that enter through the urethra

Predisposing factors of UTI

• more common in women (women have a shorter urethra, makes it easier for bacteria to reach the bladder)

• prostatic hypertrophy compresses the urethra and obstructs urine flow in older men (causes retention of urine allows bacteria to multiply)

• congenital abnormalities (in children)

• pregnancy (hormonal changes and pressure in the urinary tract can slow urine flow and increase infection risk)

  • urinary catheterization

Cystitis and Urethra manifestations

lower urinary tract infection, bladder and urethra inflamed

• hyperactive bladder and reduced capacity cause frequent urge to urinate

• pelvic area pain (subprapubic discomfort)

• dysuria, urgency, frequency, and nocturia

• systemic symptoms (fever, malaise, nausea, leukocytosis)

• urine is cloudy and unusual odor

• urinalysis → indicates bacteriuria, pyuria, and microscopic hematuria

UTIs in kids

infants → less specific and vague sings (like unexplained fever) - always check for UTIs

neonates → fever, abdominal distension, vomiting

infants → fever, feeding problems, foul-smelling urine

toddlers → abdominal pain, abnormal voiding patterns

children → classic features more common

Vesicoureteral Reflux

children with recurrent UTIs need to be evaluated for this; occurs when the distal portion ureter is congenitally short (micturition forces urine into ureter)

• normal → distal portion ureter found between mucosa and bladder muscle; flap is compressed upon micturition

UTIs and pregnancy (hormonal and anatomical)

• The hormonal and anatomical changes of pregnancy increase the risk of UTIs:

➢ Hormonal: progesterone decreases peristaltic activity of ureters

➢ Anatomical: bladder displaced compressed with uterus

• Approximately 10% of pregnant women with a UTI are asymptomatic

• Asymptomatic bacteriuria present prior to pregnancy leads to symptomatic infection

➢ Increased risk for –- pyelonephritis, toxemia

Pyelonephritis

bacterial infection of the kidneys that affects the renal pelvis and kidney tissue

➢ Infection ascends from ureter into kidney

➢ One or both kidneys may be involved.

• Purulent exudate fills pelvis and calyces

➢ Obstruction and collection of filtrate causes hydronephrosis

• Recurrent or chronic infection can lead to scar tissue formation.

➢ Loss of nephron tubule function

➢ Chronic renal failure if untreated

Manifestations of Pyelonephritis

 Signs of cystitis plus pain associated with renal disease –- dull, aching pain in lower back or flank area

 Systemic symptoms:

➢ High fever: temperature may rise above 38°C.

➢ Chills and shaking: the patient may experience shivering due to infection.

 Urinalysis – shows findings cystitis, such as white blood cells, bacteria, and leukocytes.

➢ Urinary casts are present – reflection of renal tubule involvement, not seen in lower UTIs (cystitis and urethritis)

Types of Glomerular Disease

nephritis syndromes → group of clinical disorders characterized by proliferative inflammation in glomeurli (decreases GFR)

• acute poststreptococcal glomerulonephritis

nephrotic syndrome → produces increased permeability of the glomerulus and leakage of large amount of protein into urine (gross proteinuria)

most glomerular diseases are mixrd

acute poststreptococcal glomerulonephritis (APSGN)

APSGN is most common form nephritic syndrome

➢ Occurs after an infection caused by group A beta- hemolytic streptococcus (GAS).

➢ Immune mediated: development of antistreptococcal (ASO) antibodies, formation of an antigen-antibody complex, activation of complement system

• Severe inflammatory response in glomeruli

➢ Increased capillary permeability—leakage of some protein and large numbers of erythrocytes

➢ Congestion and cell proliferation: decreased GFR— retention of fluids and wastes

pathogenesis diaphragm on slide 49

Manifestations of APSGN

• Decreased urine output – urine becomes dark and cloudy

• Facial and periorbital edema –- swelling in the face and around the eye

• Hypertension: increased blood pressure due to fluid and sodium retention.

• Flank or back pain: due to swelling and stretching of renal capsule

• Oliguria: decreased urine output.

• General signs of inflammation –- fatigue and weakness

APSGN Lab Tests

Blood tests

➢ Elevated BUN –- blood urea and creatine levels increased

➢ Elevation of anti-streptococcal antibodies: antistreptolysin, antistreptokinase

➢ Metabolic acidosis: kidneys cannot remove excess hydrogen ions and regulate bicarbonate.

Urinalysis

➢ Proteinuria, hematuria, erythrocyte casts

➢ No evidence of infection – no bacteriuria, or pyuria (post strep is not in urinary tract; it is autoimmune reaction)

Nephrotic Syndrome

Disorder characterized by excessive loss of protein in the urine due to increase permeability of glomerular capillaries

Four classic features

➢ Massive proteinuria –- 3.5 g/day

➢ Hypoalbuminemia –- due to urinary protein loss

➢ Generalized edema (caused by decreased plasma osmotic pressure with hypoalbuminemia)

• increased aldosterone secretion in response to reduced blood volume cause sodium and water retention and more severe edema)

➢ Hyperlipidemia (high blood cholestrol and compensatory syntehsis by liver)

• Lipoprotein in liver - lipiduria

diagram on slide 52

Nephrosclerosis

hypertensive glomerular disease

 Hypertensive nephrosclerosis involves vascular changes in the kidney caused by long standing, poorly controlled hypertension

 Thickening and hardening of the walls of arterioles and small arteries

 Narrowing of the blood vessel lumen results in reduction of blood supply to kidney

➢ Stimulation of renin secretion (RAAS) –- vasoconstriction

➢ Continued ischemia, destruction of renal tissue –- chronic renal failure

pathogenesis on side 55

Renal Cell Carcinoma

common primary cancer of the kidney arising from the tubule epithelium

• most commonly develops in the renal cortex, the outer part of the kidney; can metastasize to liver, lung, bone, or CNS

• usually symptomatic in early stages

• occurs more frequently in men and smokers

• treatment → removal of kidney

• tumor is radioresistant and chemotherapy is not used in most cases

Manifestations of Renal Cell Carcinoma

• Early symptom –- painless hematuria (blood in urine)

• Dull, aching flank pain

• Palpable mass in abdomen

• Unexplained weight loss

• Anemia or erythrocytosis

• Paraneoplastic syndromes

  • Hypercalcemia

  • Cushing syndrome

Wilms Tumor (nephroblastoma)

develops from immature kidney cells that have not fully developed into normal kidney tissue (germ cells in kidneys)

• childhood cancer → ages 3 to 5

• associated w/ genetic mutations affecting normal kidney development (mutations in tumor suppressor gene on chromosome 11 can increase the risk)

• aggressive cancer, but one of the most curable solid cancers in childhood (responds well to treatment)

Manifestations of Wilms tumor

• tumor grows into large abdominal mass

• abdominal pain

• hematuria

• HTN

• weight loss