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Renal- Pathophysiology

Terms in this set (68)

Renal Blood Flow
Kidneys receive 20% of cardiac output during rest; reduced to 2% to 4% during physical or emotional response
Abdominal aorta gives rise to renal arteries, which enter the hilum of each kidney; eventually branch into afferent arterioles, which enter glomerular capillary beds
Efferent arterioles leave the glomerular capillary bed; eventually converge into progressively large veins until leaving the kidney
Function of the kidney
Primary role is to maintain body fluid volume and composition and to filter waste products for elimination
Help to regulate blood pressure
Participate in acid-base balance
Produce erythropoietin for red blood cell (RBC) synthesis
Metabolize vitamin D to an active form
Hormones- endocrine role
ADH Acts directly on renal tubular cells (collecting duct and distal convoluted tubule) making them more permeable to water
When present at certain level in blood, makes kidneys conserve body water
When absent or diminished in blood, kidney loses body water
Urine Output
Adult: > 1 ml/min
Infants: > 0.5 ml/kg/hr
Children: > 1 ml/kg/hr
Oliguria: diminished urine output, less than minimal expected production rate
Anuria: no urine output
Ureters
Location: behind the parietal peritoneum
Structure: ureter expands as it enters the kidney to form the renal pelvis; subdivided into calyces, each of which contains renal papillae
Functions: collect urine secreted by the kidney cells and propel it to the bladder by peristaltic waves
Urinary Bladder
Location: behind symphysis pubis, below parietal peritoneum
Structure: collapsible bag of smooth muscle lined with mucosa arranged in rugae, three openings- two from ureters and one into urethra
Function: reservoir for urine until sufficient amount accumulated for elimination and expulsion of urine from body by way of urethra
Urethra
Female: behind the symphysis pubis, anterior to the vagina
Male: extends through the prostate gland, fibrous sheet, and penis
Structure: musculomembraneous tube lined with mucosa; opening to exterior called urinary meatus
Female: passageway for expulsion of urine
Male: expulsion of both urine and semen
Male vs. Female Urethra
Female is urethra 2.5-3.5 cm long
Allows urine to pass more freely

Male urethra 16.5-18.5 cm long
Passes through prostate
Disorders of Glomerular Disorders
Nephritic syndromes
Proliferative inflammatory response
Nephrotic syndrome
Increased permeability of glomerulus
Mixed nephritic and nephrotic responses
Chronic glomerulonephritis
Glomerular lesions associated with systemic disease
Glomerular Disorders
The glomerulus of the kidney is where filtration occurs into the nephron
Blood enters the glomerulus, and then ions, water, glucose, and other substances are filtered into Bowman's capsule of the nephron
Glomerular disorders affect the glomerulus and change the filtration properties of the kidney
Glomerularnephritis
Inflammation of the glomerulus
Can be acute or chronic
Acute glomerulonephritis is glomerular inflammation that is typically caused by group A poststreptococcal infection
Chronic glomerulonephritis is a combination of several glomerular diseases that ultimately lead to chronic renal failure

Types:
Acute Glomerulonephritis
Rapidly Progressive Glomerulonephritis (RPGN)
Chronic Glomerulonephritis
Clinical manifestations of glomerulonephritis
Proteinuria (varying degrees based on the specific disease) **
Flank or back pain
Hematuria- blood in urine
Decreased urine output
Edema
General signs of inflammation: malaise, fatigue, headache, anorexia, and nausea
HTN
Glomerulonephritis Assessment
-History of recent upper respiratory or skin infection, or invasive procedures
-Blood pressure for baseline
-Urine for Blood, protein
-Presence of dyspnea, edema, neck vein engorgement
Glomerulonephritis Therapeutic Interventions
Antibiotics such as penicillin to treat underlying infection
Dietary restriction of sodium, fluids, and protein based on clinical status
Diuretics and antihypertensive to control blood pressure
Rest; regular activity when hematuria and proteinuria resolve
Nephrotic Syndrome
clinical presentation is primarily massive proteinuria, specifically defined as 3.5 grams or greater in 24 hours
• Increase in glomerular permeability and loss of plasma proteins; can be an autoimmune disorder of the glomerular bed that can damage permeability—how it occurs in children
• Swollen from loss of plasma proteins
• Can also happen with lupus and diabetes in the older population*
Clinical Manifestations
o Severe proteinuria*
o Hypoalbuminemia*
o Edema*
o Hyperlipidemia
o Lipiduria
o Decreased vitamin D
Nephrotic Syndrome Evaluation
Evaluation
-24-hour urine collection: protein >3.5 grams
-Serum albumin <3 g/dl
• Normal is <150 mg of protein in healthy adult
• Normal serum albumin is <5 g/dl

-Fat droplets in urine
-Increase in serum cholesterol, phospholipids, and triglycerides
-Confirmation by renal biopsy
Treatment of Nephrotic Syndrome
Focuses on treating the underlying problem,
Diet and drug therapies,
Increase protein,
Salt is restricted as is fat intake
o May need diuretics to help kidneys filter fluid
o May need hypolipidemic drugs
UTI's
Bacteria usually enter through the urethra
Host defenses include:
Washout phenomenon
Protective mucus
Local immune responses and IgA
Normal bacterial flora
• Autoimmune people are more prone to fungal infections
• E-Coli** is most common type of organism in UTI's
UTI risk factors
Age extremes
Sexually active women
Patients with:
An indwelling catheter Lower urinary tract obstruction
Diabetes mellitus
Immunosuppression
UTI pathogenesis
Escherichia coli (about 80% of uncomplicated and 20% of complicated cases)
Klebsiella, Proteus
Pseudomonas, Staphylococcus saporphyticus
Candida (most common fungal)
Schistosomiasis (most common parasitic)
Urinary Tract Infections (UTI) Cystitis
Is an inflammation of the bladder wall usually caused by an ascending bacterial infection (E. coli most common)
More common in females due to: shorter urethra, childbirth, anatomic proximity of the urethra to the rectum
Occur in men secondary to epididymitis, prostatitis, renal calculi
Urinary Tract Infections (UTI) Urethritis
Is an inflammation of the urethra caused by staphylococci, E. coli, pseudomonas species, and streptococci
Although inflammatory symptoms are similar to gonorrheal urethritis, sexual contact is not the cause
May cause prostatitis and epidymitis
Urinary Tract Infections (UTI) Urosepsis
Is caused by gram-negative bacteria
May result from an indwelling urinary catheter or an untreated urinary tract infection
• Number 1 cause of septic infections- UTI's that become systemic
• If it is caused by gram-negative bacteria which is hard to treat
Urinary Tract Infections (UTI) Clinical Findings
Subjective:
Urgency; frequency; pain and bearing down on urination
Objective:
Nocturia; hematuria; pyuria (cloudy urine) ; bacterial growth evident in urine culture
UTI treatment
Identification of causative organism through urine culture
Pharmacologic therapy with antibiotics, urinary antiseptics, antispasmotics
Diet directed toward altering the properties of urine (cranberry juice)
Additional fluids to dilute the urine
Warm sitz baths to provide comfort
Pyelonephritis
It is either the presence of active organisms in the kidney or the effects of kidney infections
Acute: is the active bacterial infection
Chronic: results from repeated or continued upper urinary tract infections or the effects of such infections. Usually occurs with an anatomic urinary tract anomaly, obstruction, or vesicoureteral urine reflux
Differs from a simple UTI in that the infection in pyelonephritis occurs proximal to the bladder in the ureters, renal pelvis, and renal parenchyma
• urine back flows from bladder to kidney- congenital defect
• Chronic UTI's that cause Scarring on ureters can also cause reflux of urine
Pyelonephritis Clinical Manifestations
Fever/Chills
Tachycardia and tachypnea
Flank or back pain/Tender costal vertebral angle (CVA)
Abdominal, often colicky, discomfort
Nausea and vomiting
General malaise or fatigue
Burning, urgency, or frequency of urination
Nocturia
Tests for pyelonephritis
U/A: shows a positive leukocyte esterase and nitrate*s; occasional RBCs, WBC casts, and proteinuria may be present
Urine culture
Blood culture
IVP---Intravenous Piallegram shows any obstruction. Contrast injection showing any obstruction in the ureters.
Treatment for Pyelonephritis
-Antibiotic to treat the infection
-Fluid intake is recommended at 2 to 3L/day unless another condition requires fluid restriction
-Pain medication
-Diet with adequate calories and all food groups
Urinary Tract Obstruction
• Urethra all the way to renal pelvis (entrance of kidney- where blood vessels enter kidney) there is obstruction
• Can be due to renal calculi- kidney stone
• Neurogenic Bladder- CNS is not able to control emptying of urine.
• Cancerous tumors can cause obstruction
• Obstructive Uropathy- backflow of urine from ureters into the kidney
• It demands urgent attention and intervention because you can't eliminate urine.
• Backflow can cause enlargement of kidney/ureter.
Factors
The location of the lesion.
Whether one or both of the upper urinary tracts are involved.
The severity of the obstruction.
The length of time that the obstruction has been present.
The nature of the obstruction.
Terms
Hydroureter - abnormal enlargement of the ureter.
Hydronephrosis - abnormal enlargement of the kidney.
Ureterohydronephrosis - abnormal enlargement of the ureter and kidney.
Upper urinary tract obstructions
Variety of causes
congenital abnormalities
inflammation
tumors
metabolic conditions
Most Common
KIDNEY STONES
Pathophysiology- Calculi
Urine becomes concentrated with insoluble materials
Crystals form from these materials and then consolidate, forming calculi
Calculi remain in the renal pelvis and damage or destroy kidney tissue or they may enter the ureter
Large calculi in the kidneys may cause tissue damage
If obstruct urine flow may cause hydronephrosis
Risk factors
-Age 20-40 years
-Gender Men > Women (men: up to 20%, women: 5-10%)
-Fluid intake- Persons who do not consume adequate fluids
-Diet- Excessive vitamin D and calcium ingestion, vitamin A deficiency
-Lack of Exercise-based on underlying pathology: such as gout, Uti, Inflammatory bowel
-Geographic location-Based on temperature, humidity, and rainfall. Living in the "sunbelt" of the U.S. increases risk of kidney stones because persons tend to become dehydrated
Renal Calculi
Four types of kidney stones:
o Calcium Stones- extra bone resorption and intake of calcium. Bone loss is occurring causing calcium to deposit in kidneys
o Magnesium ammonium phosphate stones- form in alkaline urine.
o Uric Acid Stones- increase in uric acid; gout is usually presented as presentation. Uric acid is from a lot of protein
o Cystine Stones- rare; genetic kidney defect in amino acid breakdown.
Calculi
Masses of crystals composed of minerals that are normally excreted in the urine
May form anywhere in urinary tract
Usually develop in renal pelvis or calices
Causes:
-Dehydration
-Infection
-Changes in urine pH
-Obstruction
-Immobilization
-Diet
-Metabolic factors
Clinical Manifestation
Dull, aching flank pain
May travel from lower back to sides and then pubic region and genitalia
Intensity fluctuates and can be excruciating
Nausea, vomiting
Hematuria
Abdominal distention
Oliguria
Diagnosis
KUB- Kidney Urine Bladder X-ray
Ultrasound- can show kidney enlargement, stones
Urinalysis- can tell you what type of stone in might be
24 hour urine collection- try to catch stones by seeing the composition of the stone to change the patient's future dietary intake
Blood tests- rule out causes. Does patient have gout? Calcium problems? PTH abnormalities?
Treatment
90% are small and pass naturally with vigorous hydration (> 3 liters/day)
Drug therapy
-Antimicrobials
-Analgesics
-Antiemetics
Removing calculi:
-Lithotripsy
-Shatter calculi into fragments for natural passage or removal
-Cystoscope - from ureter
-Surgical removal
-Prevention:
-Fluid intake 2.5-3L/day
-Restrict: Vitamin C
Vit D, calcium
Lower Urinary Tract Obstruction
several types
may involve the bladder, bladder neck, prostate, or urethra
symptoms are related to alterations in urine excretion
• Can be due to BPH, Bladder tumors, STD's- can lead to scarring/stricture
• To compensate, the bladder becomes overly sensitive and the patient needs to go more
Manifestations of lower urinary obstruction
Daytime voiding frequency
Nocturia
Poor force of urinary stream
Intermittency of urinary stream
Bothersome urinary urgency, sometimes with hesitancy
Incomplete bladder emptying
Tumors
may occur in either the kidney or bladder- Renal tumors may be small, benign tumors that are difficult to detect, or they may be larger malignant tumors that usually arise from the proximal tubule epithelial cells
-Bladder tumors are fairly common; they are the fifth most common malignancy
Renal Cell Carcinoma
Most common renal neoplasm (85%)
Risk factors for development of RCC include tobacco use, obesity, and long-term analgesic use
Clinical Manifestations
Hematuria (most common)
Flank pain
Palpable flank mass
Weight loss
Diagnosis of renal cell carcinoma
Ultrasonography
Intravenous pyelography (IVP)
CT scan or MRI
Renal angiography-- looks at vessels of kidney
Bladder Tumors
Evaluation is made through cystoscopic exam with tissue biopsy
Other evaluative tests may include urinalysis to rule out infection, urine cytology, transurethral biopsy, and X-ray examination

Treatment:
depends on the size and type of cancerous lesion
may include transurethral resection or laser ablation, or in severe cases, radical cystectomy with urinary diversion and adjuvant chemotherapy for locally invasive tumors
Classification of Renal Failure
Renal insufficiency: occurs when renal function is impaired to 25% the normal function
Renal failure is classified into acute and chronic.
Acute renal failure is further classified into prerenal, intrarenal, and postrenal
Acute Renal Failure
The sudden inability of the kidneys to regulate fluid and electrolyte balance and to remove toxic products from blood
Usually follows trauma to the kidneys or overwhelming physiologic stress (e.g. burns, septicemia, nephrotoxic drugs and chemicals, severe shock, etc) that decreases blood flow to the glomeruli or to the nephrons
Sudden and almost complete loss of glomerular and/or tubular function
Pre-Renal Failure
Any condition leading to inadequate kidney perfusion (less than 25% of CO)
Reversible with reestablishment of adequate flow
Pre-Renal Etiology
Cardio-vascular disorders
Cardiac tamponade
Heart failure/Myocardial infarction
Hypovolemia/Hemmorhage
Burns
Dehydration
Diuretic overuse
Trauma
Peripheral vasodilation
Anti-hypertensive drugs
Sepsis
Renovascular obstruction
Tumor
Pathophysiology for Pre-Renal Failure
Diminished perfusion to the kidneys without renal tubular damage
Effect of decreased pressure to kidney perfusion is:
-Decreased pressure to renal artery
-Decreased afferent arterial pressure which diminishes forces favoring filtration
-Drop or cessation of GFR -oliguria
Intrarenal Failure
Causes
Glomerulonephritis/Pyelonephritis
Polycystic kidney disease
Diabetes mellitus
Transfusion reaction
Severe crush injury
Acute tubular necrosis

o Polycystic kidney disease-cysts all over kidneys
o DM- will eventually cause damage to tubules of kidneys
o Tranfusion Reaction- causes antibody complex which can clog up the glomerulus
o Severe Crush Injury—Cellular muscle cells will block up and decrease flow to kidneys
o Acute Tubular Necrosis- Occurs most of the time with nephrotoxic drugs. Aminoglycosides can cause tubular damage, sepsis, prolonged ischemia
o Vessels feeding kidneys become vasodilated
o Obstruction of flow by edema and cellular debris
o Can cause swelling, decreased glomerular filtration rate.
o True Kidney Damage***- true damage to nephron, tubules, glomerular bed.
Pathophysiology of Intrarenal Failure
Cortical involvement of vascular, infectious or immunologic processes
Causes renal capillary swelling and cellular proliferation
Decrease GFR occurs secondary to obstruction of glomeruli by edema and cellular debris--oliguria
Post-renal
Bladder obstruction
Anti-cholinergic drugs
Autonomic nerve dysfunction
Infection
Tumor
Uretheral obstruction
Prostatic hyperplasia or tumor
Ureteral obstruction
Blood clots
Calculi
Edema or inflammation
hemorrhage
Surgery (accidental ligation)
Tumor
Uric acid crystals
Pathophysiology of Post-Renal
Complete Obstruction:

Impediment of urine flow accompanies bilateral kidney involvement
The backup of pressure will compress the kidneys, may lead to intrarenal failure
Acute Renal Failure Clinical Findings
Subjective:
Irritability; headache; anorexia; tingling of extremities; lethargy and drowsiness that can progress from stupor to coma
Objective:
Sudden dramatic drop in urinary output appearing a few hours after the causative event
Restlessness, twitching, convulsions
Nausea and vomiting
Clinical Manifesations
Azotemia
Elevated blood urea nitrogen
Elevated serum creatinine
Metabolic Acidosis---
Unable to excrete H+
Unable to conserve bicarbonate
Decrease urine output/
Dilute urine
Electrolyte Imbalance
Excess salt and water retention if normal salt intake
Hyperkalemia
Low serum calcium
Anemia
Deficiency in erythropoietin production-
Decreased RBC life span
Hypertension
Therapeutic Interventions
Correct the underlying cause of renal failure
Altering medication dosages
Dialysis
Diet therapy-Calories adequated to prevent tissue breakdown: 2000 to 2500 (protein low, high carb for energy, moderate fat)
Sodium controlled/Low potassium
Calcium supplements
Nursing Interventions
Daily weights
Assess serum electrolytes
Signs of hyperkalemia and hyponatremia
Monitor intake and output
Provide special skin care to prevent breakdown
Diagnosis
History and physical
Urine
Fixed specific gravity/Protein
Diagnostics:
Renal ultrasound
CT
IVP
Renal biopsy
Blood work:
Hyperkalemia
Hyponatremia
Hyperphosphate
Hypocalcemia
Increased BUN, Cr
Metabolic acidosis
Anemia
Chronic Renal Failure
The progressive inability, over months to years, of the kidneys to respond to changes in body fluids and electrolyte composition with an inability to produce sufficient urine
Results in gradual tissue destruction and loss of kidney function
Occassionally results from rapidly progressing disease of sudden onset
Patho of chronic renal failure
Gradual loss of entire nephron units
Functional capacity of entire nephron is lost and renal mass is reduced → progressive deterioration of glomerular filtration, tubular secretion and reabsorption
Eventually the kidneys are unable to excrete metabolic waste and regulate fluid and electrolyte balance
Development of CRF
Diminished renal reserve
Nephrons are working as hard as they can
Renal insufficiency
Nephrons can no longer regulate urine density
Renal failure
Nephrons can no longer keep blood composition normal
End-stage renal disease
Manifestations of CRF
Hypervolemia
Labs same as ARF
Azotemia
Metabolic acidosis
Anemia
Peripheral neuropathy
Uremic frost-deposit of waste on the skin, distinct odor, it looks like frost on the skin'
Treatment of CRF
Supportive care
Conservative measures
Low protein diet (unless on PD)
High calorie diet
Na+ and K+ restrictions
Fluid restrictions
Drug therapy
Loop diuretics
Antihypertensives
Sodium bicarb, calcium carbonate, phosphate binding agents, calcium supplements, vit D
Iron and folic acid supplements, Epogen
Dialysis
Hemodialysis
Peritoneal dialysis
Transplant
Uremia
Renal filtering function decreases
Altered fluid and electrolyte balance
Acidosis, hyperkalemia, salt wasting, hypertension
Wastes build up in blood
Increased creatinine and BUN
Toxic to CNS, RBCs, platelets
Dialysis
• Stick catheter into abdominal cavity and put in fluid, allow it to dwell, and the membranes of the abdominal bed act as a filter, fluid gets exchanged in capillaries, leaks out, and then they suck it out with gravity.
• Fluid gets drained from peritoneal
• Infection* is a risk factor
• Ascites*- Peritonitis
• Can puncture an organ
• Respiratory Distress- (If you have respiratory distress, drain right away)
• Fistula- arterial/venous is how the patient is dialised
• Or can be dialized via central line.
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