Disorders of kidneys and urinary tract function

Urinary tract function

Produces, Stores, and eliminates urine

Composed of bladder, two kidneys, two ureters, and the urethra

Kidneys

• Responsible for homeostasis via urine production and elimination

• Body functions impacted

  • Blood pressure

    • the problems with kidney first thing that happened is impact with blood pressure because the kidney secretes renin

    • Secondary hypertension is when the kidney overproduces renin

  • Electrolyte and acid-base balance

  • RBC production  

    • Kidney secretes the hormone erythropoietin that causes the bone marrow to create more RBCs

  • Bone health

Acute Kidney Injury (AKI)

Rapid decrease in kidney function

Chronic Kidney disease (CKD)

Loss of kidney function over time, Results from a failure of the body to remove waste products

End stage renal disease (ESRD)

Occurs if CKD is not treated. Results from failure of the body to remove waste products (need dialysis)

Concepts related to disorders of kidney and urinary tract function

Elimination of waste products (at the glomerulus area): without blood flow to the kidneys, urine output decreases

Acid base balance

• Bicarbonate acts as buffer to maintain acid-base balance

• In acidosis, kidneys reabsorb bicarbonate

• In alkalosis, kidneys excrete more bicarbonate

Role of kidneys in acid base balance

Glomerulus: where the blood is filtration happens to eliminate toxin waste products and in the nephron and the pct is where everything that is filtrated that needs to stay in the body like glucose they can be reabsorbed in the pct

Collecting duct: where extra water or sodium is reabsorbed where most of the normal activity to absorb water and sodium. When sodium is reabsorbed the body looses potassium so a problem with this the body ends up with high potassium and any extra H ions there is an extra secretion for the nephron

Water is reabsorbed in the descending loop and the ascending loop reabsorbed bicarbonate if there is a need, if the blood is alkaline and is not reabsorbed then the ascending loop will reabsorb the bicarbonate

Glomerular disorders- etiology and pathogenesis

Glomerulonephritis (GN)

• Inflammation of the glomeruli and capillaries

• Characterized by proteinuria (protein in the urine), hematuria (increased blood in the urine), and edema (loss of protein (albumin) in urine the ability to keep osmolarity decreases and causes water to accumulate in interstitial space)

• primary cause of AKI and CKD

Etiology and pathogenesis

• Postinfectious

  • An infection is specific area of the body the infection could induce the formation of immune complex (hypersensitivity 3 the formation of immune complex) this complex eliminated and goes to the kidneys so it can possibly get stuck in the kidney (accumulation of immune complex)

• Systemic disease 

  • Kupus or diabetes

• Toxin exposure

  • Because they are responsible for elimination

• Thrombosis

• Genetic

Pathophysiology

• The infection triggers the immune system to attack the kidneys, leading to inflammation and damage to the glomeruli. This process can result in symptoms such as hematuria, edema, and hypertension, and may progress to acute kidney injury. This condition is characterized by the presence of immune complexes in the glomerular basement membrane, which can lead to glomerulonephritis

Diagnosis

• Biopsy

Treatment

• Blood pressure control (causes less filtration rate)

• Blood cholesterol control

• Control of rising creatinine: immunosuppression

  • Creatine is a bioproduct of protein that eliminated through the urine so controlling the rising when you have an increase in urine creatine is an extra filtration of protein the best is to stop inflammation that is with glucocorticoids to create immunosuppression

Clinical manifestations of nephritic syndrome

Hematuria (characterized by blood in the urine), mild proteinuria, RBC casts/dysmorphic RBCs

Clinical manifestations of nephrotic syndrome

Hyperlipidemia

• Decrease in blood protein and decrease in blood and increase in lipid in urine

Hypoalbuminemia

• Due to decrease in proteinuria. So this means the protein is in the blood is decrease because of the increase in urine

Edema

• The accumulation of fluid in interstitial space because there is a decrease in blood meaning osmotic pressure is declined

Urinary fatty casts

etiology and pathogenesis diabetic nephropathy

CKD resulting from hyperglycemia

• Leading cause of End-stage renal disease (ESRD)

• Proteinuria and hyperfiltration

• Risk factors

  • Poor glycemic control

  • Uncontrolled hypertension

  • Obesity

  • Smoking

  • Genetic factors

  • Race

    • More prevalent in African American, Hispanic, American Indian, and Asian individuals

Progression of disease

• Hyperglycemia → Polyuria → Increased renal blood flow → Glomerular hypertrophy → Glomerular hypertension → hyperfiltration

  • First is hyperglycemia and because it is high it will increase osmolarity in filtrate and if there is to much glucose that will make the filtrate more concentration and making you urinate more (polyuria) that cause renal blood flow increase and will induce the nephrosis will cause more cells being produced/divided on the glomerulus the filtrated rate will decrease this means kidneys secretes renin and adapt vascular to increase blood in glomerulus leading to hypertension to then lead to hyperfiltration due to more blood flow

Diabetic nephropathy

A leak in the protein the albuminuria is the main cause and no present of RBC in the beginning stages

Clinical manifestations

• Albuminuria (you have a problem on glomerulus filtration)

• hyperfiltration

• Hypertension (constriction of the efferent artery is increasing glomerulus pressure)

Diagnosis

• Renal biopsy may not be necessary

• Diabetes (hyperglycemia), hypertension, and albuminuria leads to diagnosis

Treatment

• Maintain BP <140/90 mmHg

  • Ace inhibitors

  • ARBS angiotensin receptor blockers control the formation of angiotensin 2

• Blood cholesterol control

  • Statins

• Maintain A1C <7% (glycated hemoglobin, marker for chronic blood glucose, want to keep it low)

  • Lifestyle modifications

  • Glucose lowering medications

Hypertensive nephropathy

CKD resulting from long-standing hypertension

• Second leading cause of ERSD (end stage renal dysfunction)

• Affects glomerulus, tubules, and vasculature of kidneys

  • Leads to nephrosclerosis (the thickness and inability of vasculature in kidney to constrict and dilate (no longer control pressures))

• Risk factors

  • Genetics

  • Diabetes

  • Previous renal disease

  • More prevalent in African Americans

Possible etiologies of essential hypertension

• Genetics

• Lifestyle choices (good diet and constant exercise that will avoid this)

• Activation of RAAS (system increase blood pressures)

• Arterial stiffness (ability to constrict and dilate)

Clinical manifestations

• Left ventricular hypertrophy

  • Need more force from the heart to pump blood so there is a problem with BP)

• Opthalamic changes (arteriovenous nicking, retinal hemorrhage) (eye problems)

• Mild proteinuria

• Increased BUN and creatinine over time

  • BUN = Blood urea nitrogen

  • Because glomerular filtration rate decreases

Diagnosis

• PMH, hypertension, increased BUN/creatinine

Treatment

• Maintain BP <140/90 mmHg

  • ACE inhibitors

  • ARBS

• Blood cholesterol control

  • Statins

• Lifestyle modifications

  • Regular exercise

  • Smoking cessation

  • Maintain BMI <25

  • Restrict dietary sodium to <2.4 grams/day

Activation of RAAS

Atherosclerosis → Reduction of blood flow to the glomeruli → SNS stimulation → Activation of RAAS → Renal renin production → Increase systemic BP

Atherosclerosis in kidney causes reduction of blood flow and the stimulant for the nerve system that will increase the secretion of renin and aldosterone to increase sodium retention to then increase BP

UTI

Infection of lower urinary tract of the bladder, upper urinary tract, or the kidney

• Females more likely because you have urinary canal production next to anus

• bacterial infection that need medication to control infections becuase it can migrate to kidneys

Diagnosis

• based on clinical symptoms

• Urinalysis and culture

Treatment

• Antibiotic therapy

Cystitis

Infection of the bladder

Most common bacterial infection

Risk factors

• Diabetes mellitus

• Familial predisposition

• Obstruction (kidney stones)

• Neurogenic bladder

• Use of spermicides and diaphragms (during intercourse)

Pyelonephritis

Infection of the renal pelvis and parenchyma (walls of kidney) 

Risk factors 

• Female gender

  • Sexually active

  • Use of spermicides or diaphragm

  • Pregnancy

• Genitourinary tract abnormalities

• Neurogenic bladder

• Immunosuppression

• Diabetes

Middle portion of the kidney a nd this is the area that gets infected (major calyx)

Ascending bacterial colonization from urethra to bladder

Most caused by E.coli

Classified as complicated or uncomplicated

Other causes

• Obstruction in the flow of urine

  • Stones

  • papillary necrosis

• Residual urine retention

• Bacteremia (pyelonephritis)

• Instrumentation (invasive procedure in the kidney)

• Back flow of urine (causes accumulation of bacteria)

  • Vesicoureteral reflux (VUR)

Cystitis

Clinical manifestations

• Dysuria (pain during urination)

• Urgency

• Frequency

• Confusion (older adults)

Diagnosis

• based on clinical symptoms

• Urinalysis

• Urine culture as needed

No fever because you don’t have inflammation that effects the blood stream the inflammation is in the urinary bladder

Pyelonephritis

Clinical manifestations

• Costovertebral angle pain

• Fever

• Chills

Diagnosis

• Urine culture

• CT scan

  • Tells you if you have inflammed kidney

More vascular so you have inflammatory process to induce a fever, white blood cells in the urine

Renal calculi

Nephrolithiasis (kidney stones)

• Results from formation of urinary crystals into larger stones

• Common obstruction

  • Usually affecting white males

• Risk factors

  • Previous stones

  • Dehydration (what makes a kidney stone)

  • Hypercalcuria (increase calcium in the urine)

  • Hyperoxaluria (oxalate component that if you eat to much nuts/peanuts or spinach)

  • High-sodium diet

• Composition

  • Majority are calicum based

  • Less common: uric acid (waste product induce a stone), Struvite (mineral magnesium), cysteine stones

• Stone formation

  • Damage to the lining of the urinary tract

  • Crystal aggregation (blockage of urinary tract and more mineral get accumulated)

  • Slow urine flow to allow crystallization

  • Excretion of large amounts of calicum (in urine)

• Clinical manifestation

  • Acute, unilateral flank pain (only one kidney stone in one kidney never both)

  • Nausea

  • Vomiting

  • Severe pain that comes and goes (renal colic) 

    • Comes and goes because stone moves

• Diagnosis

  • Based on clincal symptoms

  • Ultrasound

  • X-ray

• Treatment

  • Thiazide diuretic (will make you pee) or allopurinol

  • Surgery as needed

  • Percutaneous Nephrolithotomy: this induces a small tube in the kidney to aspirate kidney stone or breakdown the stones

Development of kidney stones within urinary tract

Kidney stones happen in minor or major calyx

Can be in ureter or urethra

Uric acid kidney stone starts a large blockage in the kidney so it is classified as such and will block urinary tract

Urinary incontinence

Most common in Caucasian women

Risk factors

• Pregnancy

• Older age

• Obesity

• Hypertension

• Smoking

• Alcohol consumption

• Postmenopausal diabetes

• Neurogenic bladder

Diagnosis

• Report of loss of urine in various situations

Treatment

• Weight loss

• Bladder training

• Pelvic floor muscle training

• Pessary

• Surgery

• Antimuscarinics/anticholinergics

Stress incontinence

Physical activity

Sneezing

Coughing

urgency incontinence

Feeling urgency with loss of urine

postural incontinence

Position change

Nocturnal enuresis

During sleep

Mixed incontinence

Stress, urgency, or postural features

Continuous incontinence

Continuous loss of urine

Insensible incontinence

Unawareness of loss of urine

Coital

Occurs with Coitus

CKD

Either kidney damage of GFR (decrease) <60 mL/min/1.73 m2 for 3 months or more

Incidence continues to rise in U.S. and worldwide because of diabetes and hypertension

25% starting dialysis die within the first year of treatment

Diagnosis

• National kidney foundation guidelines

• Blood and urine tests

• Additional laboratory tests

  • Liver profile

  • Thyroid function tests

  • Electrolyte panel

  • Imaging

    • KUB (image of kidney, ureter, and bladder)

    • Renal ultrasound, arteriogram, CT, MRI

Etiology: Diabetic nephropathy

Pathogenesis

• Most frequent cause of CKD in ESRD

• Moderate albuminuria = early indicator

• Basement membrane thickening, mesangial expansion, increased glomerular permeability, decreased GFR

Etiology: Hypertensive nephrosclerosis

Increased pressure in the glomerulus → damage of glomerular cells → glomerulosclerosis

Damage of small vessels in kidney → inadequate blood supply → decrease BP to glomeruli → glomerulosclerosis

Hyperfiltration → thickening of glomerular vessels

Etiology: Chronic glomerulonephritis (infection at glomerulus)

Direct injury to the glomerulus

pathogenesis similar to diabetic nephropathy

Antibody deposition → glomerular inflammation

Chemokines and cytokines → mesangial cells promote inflammation

Polycystic kidney disease (genetic condition)

Onset begins at 30 years of age

Another cause of CKD and 3rd cause of ESRD

Cysts develop from collecting duct of nephron

Cysts increase in number and size with age

Macrophage infiltration, neurovascularization, progressive fibrosis, and decreased renal function

90% caused by mutation of PKD1 gene

Removing kidney is an option

These pt. are first line for kidney transplant

Complication: Cardiovascular disease

Manifestations

• Most common cause of death in CKD

• HTN, dyslipidemia, and chronic inflammatory state

• Secondary HTN-kidney issue

Complication: Metabolic acidosis

Manifestations

• In CKD, kidneys retain H+ ions cannot reabsorb bicarbonate

• Decreased kidney function leads to increased ammonia and retain H+ ions

• Decreased Kidney function decreases resorption of sodium bicarbonate

Complication: Chronic kidney disease-mineral and bone disorder

Manifestations

• Bone disease in CKD resulting from mineral and hormonal changes

• Causes bone pain, deformities, and fractures

• Results from abnormal bone turnover, hypocalcemia, hyperphosphatemia, and hyperparathyroidism

• Any problem in kidney leads to bone disorder

Complication: Anemia

Manifestations

• Decreased erythropoietin then you don’t have the hormone to tell bone marrow to make RBC

• Worsens with worsening CKD

• Leads to increased cardiac preload, decreased afterload, and increased cardiac output

Complication: Hyperkalemia

Manifestations: Develops as oliguria develops

Results from decreased aldosterone secretion and decreased excretion of potassium (happens in the collecting duct)

Hypervolemia

Once GFR falls, renal secretion of sodium and water decreases

Exacerbates CVD and LVH

Complication: uremia

Manifestation

• Results from waste product accumulation

Stage 5 CKD

You’re in renal failure and start dialysis

Treatment: Anti-hypertensives

Description: ACE/ARB medications

treatment: Lipid lowering agents

Description: Statin therapy

Treatment: Hemodialysis

Description: Removal of toxins and excess fluid from the blood

Blood is collected through the system and have blood pass through dialysis fluid and blood returns to body without waste products

treatment: Peritoneal dialysis (risk of infection)

Description: Removal of toxins and excess fluid by utilizing the peritoneum (collection of fluid)

Dialysis fluid just passes through perineal cavity

Treatment: renal transplantation

Description: Encouraged in those who have the potential of a good quality of life after transplantation

Very hard to transplant kidney through the back so its placed through the abdomen it’s also easier to connect the ureter that way

Diagnosis and treatment of CKD

At first stages of CKD you need to control BP so use those meds, decrease lipid, if these don’t work start dialysis 2-3/week blood is filtered