Renal System: Structure, Function and Blood Flow

Renal Structure/Function

• Kidneys' primary functions include acid-base balance, water removal, erythropoiesis, toxin removal, blood pressure regulation, electrolyte balance, and vitamin D activation
• A nephron consists of the glomerulus surrounded by Bowman's capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct leading to urination

Renal Blood Flow

• The flow starts from the renal artery to the afferent arteriole, then to glomerular capillaries, followed by the efferent arteriole, and finally to the peritubular capillaries

Regulation of Renal Blood Flow

• Autoregulation maintains a stable glomerular filtration rate(GFR) despite blood pressure fluctuations
• Sympathetic nervous system activation regulates blood flow during stress or low blood pressure
• Juxtaglomerular complex regulates renal blood flow by responding to low sodium concentration in the filtrate and stretch of the afferent arteriole
• The Renin-Angiotensin II system releases renin from juxtaglomerular cells, leading to angiotensin II formation, constricting the efferent arteriole to maintain GFR
• Nitric Oxide acts as a vasodilator
• Prostaglandins help regulate blood flow

Labs for Renal Function

• Creatinine waste product from muscle metabolism; elevated levels signals impaired kidney function
• Blood urea nitrogen (BUN) measures urea levels; high levels suggests kidney dysfunction or dehydration
• Hemoglobin/hematocrit assesses anemia, which can occur in kidney disease due to decreased erythropoietin production
• Urinalysis elevations in urine composition; urine shouldn't have glucose, proteins (albumin), or blood bacteria
• pH measures kidneys' ability to concentrate urine
• GFR estimates kidney function based on creatinine, age, race, and gender
• Creatinine clearance compares urine creatinine to serum creatinine to assess kidney filtration efficiency

Glomerulonephritis

• Glomerulonephritis is an inflammation of the glomerulus
• Glomerulosclerosis is an increase in extracellular matrix and thickening of the glomerular capillary membrane
• Glomerulonephritis is categorized by disease progression (acute, rapidly progressive, or chronic) and clinical presentation (nephrotic or nephritic)

Nephritic Syndrome

• Pathology involves acute inflammation causing occlusion of the glomeruli and damage to capillary walls
• Signs and Symptoms include decreased GFR, oliguria, hematuria, edema, and small amounts of proteinuria
• Primary causes include acute post-infectious glomerulonephritis and secondary causes such as systemic disease (lupus)

Nephrotic Syndrome

• Pathology includes glomerular damage causing increased permeability and massive loss of plasma proteins (proteinuria)
• Proteinuria leads to edema due to loss of protein in the urine; a loss/lack/absence of albumin leads to decreased oncotic pressure
• Hyperlipidemia occurs as a compensatory mechanism for albumin loss, the liver increases protein synthesis
• Foamy urine is caused by protein in the urine
• Loss of immunoglobulins and complement increases the risk of infection
• Loss of proteins for binding to drugs and hormones causes hypocalcemia
• Primary causes include glomerulonephritis and glomerulosclerosis
• Secondary causes include lupus and diabetes mellitus

Acute (post-infectious) Glomerulonephritis

• Cause involves glomerular inflammation post-infection (most commonly strep, but also staph and viral)
• Type III hypersensitivity occurs as antigen-antibody immune complexes deposit in the glomerulus, triggering inflammation, activation of complement, and release of inflammatory mediators
• Consequences include glomerular damage, cell proliferation, decreased GFR, and increased glomerulus permeability
• Signs and symptoms usually occur 7-12 days post-infection; most common in children
• Decreased GFR leads to oliguria, sodium/water retention, edema, and hypertension
• Increased permeability leads to hematuria (blood in the urine) and proteinuria (protein in the urine)

Rapidly Progressive Glomerulonephritis

• Cause involves a rapid decline in renal function that is either idiopathic (often), due to an immune disorder (lupus), or immune-mediated damage to glomerulus
• Antibodies attack the glomerular basement membrane
• Immune complexes deposit in the glomeruli causing inflammation after streptococcal glomerulonephritis
• Fibrin and macrophages accumulate, forming crescent-shaped lesions in Bowman's space, leading to rapid loss of kidney function
• Hematuria (blood in the urine) is a sign and symptom
• Renal failure is a consequence

Diabetic Glomerulosclerosis

• Most common cause of chronic kidney disease in the U.S
• Increased glucose in the blood results in increased filtration pressure, thickening the glomerular capillary membrane (sclerosis)
• Increased glucose leads to increased blood flow and filtration pressure, enlarging glomerular capillary pores incorporation of glucose into glomerular tissue
• Tubular endothelial cells increase reabsorption proteins, which damages the nephron
• Microalbuminuria is the first sign, followed by non-nephrotic proteinuria, nephrotic syndrome, and chronic kidney disease
• Treatment and prevention include controlled blood glucose and hypertension
• Monitoring of renal function (GFR) and serum K+ is required

Hypertensive Glomerulosclerosis

• Pathophysiology involves hypertension leading to sclerotic changes in the glomerulus and arterioles narrowing blood vessels
• Changes in kidney structure from changes to glomerular structure/function, decreased kidney size, and decreased perfusion to the kidney which leads to ischemia and tubular atrophy
• Risk factors/populations include severe high BP, African Americans, and other diseases that affect the kidneys
• Can lead to end stage renal disease (ESRD)

Chronic Glomerulonephritis

• Glomerular disease with a progressive course leads to renal failure
• Final stage of various glomerular diseases
• Consequences include renal failure and sclerosis of glomeruli
• Signs and symptoms include hematuria, proteinuria, and progression to end stage renal disease (ESRD)

Congenital Renal Disorders

• Agenesis is the absence of one or both kidneys
• Hypoplasia refers to small size of kidney; renal failure if bilateral Horseshoe kidney: fused at the midline; often asymptomatic
• Polycystic kidney disease involves fluid-filled cysts obstructing kidney function
• Autosomal dominant is the most common adult polycystic disease
• Autosomal recessive is rare, severe, with prenatal onset
• The pathophysiology defect in cell membrane proteins of the tubular epithelial cells and enlarged kidneys due to cysts
• Signs include pain, hematuria, UTIs, and possible renal failure

Renal Failure

• Acute kidney injury defined as a sudden and rapid decline in kidney function with high mortality
• Kidneys are unable to regulate fluid, electrolyte, and acid-base balance or remove wastes and is common in acutely or critically ill patients
• Chronic kidney disease defined includes renal insufficiency and end-stage renal disease
• Azotemia is an accumulation of urea (BUN) and creatinine
• Uremia is a syndrome with elevated BUN/creatinine, fatigue, anorexia, N/V, pruritus, muscle cramps, weight gain, and edema
• Pre-renal failure caused by impaired blood flow and decreased GFR from hypovolemia, shock, heart failure, or drugs
• Intrarenal failure caused by damage to kidney tubules from toxic agents or acute renal ischemia
• Postrenal failure caused by obstruction to urine flow from stones, strictures, or prostate enlargement

Acute Tubular Necrosis (ATN)

• ATN is injury and destruction of tubular epithelial cells and is commonly intrarenal
• Acute tubular necrosis can be caused by toxins or ischemia
• The Onset Phase is the progression from the injury by the hour or day, depending on cause and health
• Oliguric (maintenance) Phase characterized by damage to tubular cells, cell swelling, injury necrosis, decreased urine production, fluid retention, increased BP, elevated BUN/creatinine, and hyperkalemia
• Recovery (diuretic) Phase involves tubular epithelial repair, excessive diuresis, and possible development of chronic renal failure or ESRD
• Know the Signs and Symptoms, including increased creatinine and BUN, oliguria, anuria, electrolyte abnormalities, weight gain and edema, and uremia

Acute Kidney Injury Diagnosis and Treatment

• Diagnosis Creatinine, BUN, electrolytes, and urinalysis
• Testing: I & O, daily weights
• Treatment includes identifying and treating the cause

Chronic Kidney Disease

• Chronic Kidney Disease is progressive irreversible damage with GFR < 60 mL/min/1.73 m^2 and affects 1 in 9 Americans
• The kidney usually balances sodium and water well but that doesn't happen with CKD, leading to fluid retention
• Increased RAAS activity causes more fluid to accumulate
• Albuminuria results from damaged glomeruli that leak albumin into urine
• The kidneybalances sodium and water, but with CKD, it can't
• Decreased immune response from the kidneys inability to excrete toxins

Chronic Kidney Disease cont.

• CKD causes uremic toxin buildup, atrophy of muscle leading to Restless Leg Syndrome
• Fluid overload from CKD will increase strain on the heart leading to left ventricular hypertrophy (LVH) and congestive heart failure (CHF)
• CKD causes failure to activate vitamin D, which is needed for calcium absorption, which leads to low calcium levels, muscle cramps and bone weakness
• Parathyroid hormone (PTH) breaks down bones to release more calcium as Kidney function fails to control calcium
• Kidneys produce erythropoietin (EPO), which stimulates RBC production (erythropoiesis)
• CKD reduces ability to excrete H+ and reabsorb HCO3– to maintain acid/base balance
• CKD makes kidneys lose their filtering ability
• Treatment includes fluids/electrolytes, nutrition, monitoring drugs, renal replacement therapy, and preventing development in at risk populations

Chronic Kidney Disease management

• Recombinant erythropoietin stimulates bone marrow and helps treat underlying anemia
• Phosphate binding agents to help excrete phosphate, so that calcium levels will go up
• Renal diet: protein restriction, calories, salt/K+/phosphorus restrictions
• Management of hyperkalemia: diuretics, insulin
• Hemodialysis inidcations: hyperkalemia, very high BUN/creatinine, fluid overload, mental changes
• Hemodialysis contraindications: hypotension, coagulopathy, lack of vascular access
• Be cautions of nephrotoxic Drugs
• Avoid No NSAIDS

AB Imbalance

• Importance of acid base balance stems from its effect on physiological functions and metabolic activities
• Normal serum pH: 7.35 to 7.45
• Low pH means H is high (H+ is acidic)
• Blood buffer is 1st line of defense, Bicarbonate system most important in plasma (H2CO3=carbonic acid, NaHCO3 = sodium bicarbonate
• Respiratory regulates pH by getting rid of or retaining CO2
• The lungs regulate CO2 in minutes as urine production is the renal compenstation
• Signs and symptoms vary by acidosis and alkalosis presentation

Acidosis vs, Alkalosis

• Acidosis has CNS depression which can lead to CV issues, hyperkalemia shift
• Alkalosis has CNS overstimulation, coronary vasospasms, dysrhythmias
• Metabolic acidosis (too little HCO3-) treatment
• Respiratory acidosis (too much CO2) Labs: pH=less than 7.35, PaCO2
• treatment: correct cause, may give NaHCO3
• The body tries to reduce excess H+ by shifting it into cells

Normal Micturition

• The bladder muscles and systems perform micturition to empty the waste
• Filling and storing (SNS controls)-> Kidneys produce urine, stretches bladder (detrusor): Internal and external sphincters
• Micturition Voiding phase (PNS)-> bladder reaches 200 ml, stretch receptors send signals: Urine to exit via urethra Post void (bladder relaxes, sphincter contract)
• Problems with any of these processes can result in disorder.

Renal disorders

• Renal/ureter obstruction causes obstruction, stones, tumors
• Bladder causes prostate, organ prolapse, neurogenic bladder all causing issues to kidneys Consequence of obstruction: infection, calculi, pressure decrease GMR renal calculi- crystals formation in urinary tract which is increased by increase fluid

Renal Calcui

• increased by fluid intake Patho- stones formation in urinary tract Type of stones Calcium (75%)- avoid high dietary intake Struvite stones: magnesium-ammonium-phosphate Uric acid stones: associated with gout less than 5mm may pass, acute pain, vomitting with all stones

Benign Prostatic hyperplasia

• Enlargement of tissue and gland = obstruction
• Combination of aging , hormones all block the flow of urine.
• Decrease in force urine flow, in complete empty of bladder urgency issues

Neurogenic bladder

• Damage to neurological damage causing urination problems - stroke, spinal Types :
• spastic Bladder. At or above C2 the bladder contracts and forces all urine out
• Flaccid bladder is below S1 which cant contrated resulting in static urine Incontinence is involuntary loss/leakage of urine

Incontinence and infections

• Risk factor Problem inc. with age, diuretics, confusion and more
• Patho over Active Bladder - strong urge to urge to urinate
• Hemauria related infections E-coli-most Filaments adheres to catheters or urinary trace Bacterimia
• catheter are related to infections

Urinary tract infection (UTI)

• Wash out phenomenon - wash bacteria during pee
• Pyronphritic Upper UTI with kiddie and high levels of swelling, fever Risk factor for UTI
• obstruction, reflux, pregnancy BPH for Diagnoses: check urine and blood

Renal and reproductive system

• Wilms Tumor: common in kids 3-5 genetic
• Erectile dysfunction Blood flow is the mechanism Treatment: medications or flow increase flow Hydrocele and variocele are different issues

Variocele vs hydrocele

• Variocele
• Variocele-inflammation/dilationofveinsin scrotom , with absent values and increase blood Hydrocele
• Issue within scrotum, bilateral with possible infections issues
• Testicular torsion ( testical twisting) testical cancer
• Germ cell tumor

Reprouctive Prostitis and others

• Microbes are found in infection
• Prostatitis is inflammation of gland with uti Proctodynia - autoimmune issues of this Prostate Cancer: genetic mutation
• Uncrolled grow orginiates gland , check urine check blood and radiate to treat
• Meds to decrease swelling
• Cultural and sensitivity to see what is causing