Disease paths - renal disorders - exam 4

why do kidneys matter

-filtration = filter blood + urine formation

-waste removal = excrete urea, creatinine, meds, toxins

-fluid balance = adjust water handling to influence blood volume and pressure

-electrolyte balance = regulate potassium, sodium, phosphate, calcium

-acid-base balance = help maintain physiologic pH through bicarbonate and hydrogen ion handling

-endocrine effects = influence BP, RBC production, vit D activation

Kidney and Urologic Anatomy

-Kidneys = filter blood and produce urine

-Ureters = carry urine from the kidneys to the bladder

-bladder = stores urine until voiding

-urethra = provides the exit pathway from the body

*Obstruction anywhere along the pathway can reduce urine flow and damage the kidney.

nephron

*filtration, reabsorption, secretion

nephron flow:

1.glomerulus = high pressure filtration begins here

2.proximal tubule = large amount of water, sodium, glucose, and other solutes are reabsorbed

3.loop/ distal tubule = further adjustment of electrolytes and acid base status occurs

4.colleccting duct = final urine concentration is influenced before excretion

*when GFR falls, fluid and wastes are less effectively cleared from the blood

regulatory & endocrine roles of the kidneys

-RAAS/ BP control = the renin-angiotensin-aldosterone sodium and water reabsorption and

helps maintain blood pressure

-acid-base balance = hydrogen ions are excreted and bicarbonate is regulated to support physiologic pH

-erythropoietin = kidney releases erythropoietin to stimulate RBC production

-vit. D and calcium = vit D activation, supports calcium balance, dysfunction contributes to bone problems

basic pathophysiology of renal dysfunction

3 categories

1.prerenal = reduced perfusion

2.inrarenal = nephron/ tissue dmg

3.ppostrenal = outflow/ obstruction

*what all 3 have in common:

-kidneys are vulnerable because they receive a large blood flow and have major metabolic demands

-when blood flow, nephron structure, or urinary outflow is disrupted, filtration falls and wastes accumulate

-renal dysfunction can be acute, chronic, reversible, or progressive depending on the cause

acute kidney injury and chronic kidney disease

AKI = develops over hours to days, sudden loss of kidney function with rising waste products and possible oliguria, prompt identification of perfusion problems, direct nephron injury, or obstruction can make AKI reversible

CKD = develops gradually over months to years as nephron loss accumulates, CKD is a major public health problem and an important cause of kidney failure, complications build over time: fluid overload, electrolyte abnormalities, anemia, bone/ mineral disorders, and eventual need for renal replacement therapy

how impaired renal function becomes visible at the bedside

-Edema and Weight Gain = Reduced filtration and sodium/water retention increase interstitial fluid

-Electrolyte Abnormalities = Potassium imbalance is especially important because of cardiac risk

-Changes in Urine Output = Oliguria is common in AKI; proteinuria or hematuria suggests glomerular injury

-Waste Retention/ Uremia = BUN and creatinine rise as clearance falls

-Blood Pressure Changes = RAAS activation and fluid retention can raise BP

-Acid-Base Problems = Impaired acid handling contributes to metabolic derangements

Assessment Priorities and Risk Factors

-History Questions = Urine color or odor changes? Blood in the urine? Frequency, urgency,

dysuria, or retention? Abdominal or flank

pain? Amount of urine and pattern over time? Medication exposure or nephrotoxins?

-Risk Factors = Nephrotoxic medications or

substances. Systemic illnesses and infections. Long-standing hypertension and

diabetes. Recent surgery, trauma, dehydration or obstruction.

-Nursing Focus = Trend intake and output, daily. weights, and BP. Review the urine itself: color, blood, protein, sediment, amount. Watch for pain at the costovertebral angle, edema, or signs of infection.

Diagnostics:

Urinalysis, BUN, Creatinine

-Urinalysis = Color, clarity, and specific gravity provide clues. Blood suggests infection, stones, or glomerular injury. Proteinuria is especially important in glomerular disease and nephrotic syndrome. Nitrite or leukocyte esterase suggests infection

-Blood tests = BUN rises with reduced clearance, but dehydration can also elevate it. Serum creatinine is a more reliable indicator of kidney function. Creatinine clearance estimates GFR

Diagnostics

imaging and biopsy

-ultrasound and CT help identify hydronephrosis, stones, or obstruction

-renal biopsy provides definitive information in selected glomerular disorders

management overview before dialysis

immediate priorities

-correct fluid, electrolyte, and acid- base imbalances

-support blood pressure and perfusion

-control blood glucose when relevant

-treat the underlying cause quickly - infection, dehydration, obstruction, nephrotoxins, etc.

-when homeostasis cannot be maintained, renal replacement therapy becomes necessary

management overview before dialysis

why medication and fluids may help

-fluids can improve kidney function is poor perfusion is the problem

-diuretics may reduce volume overload when the pt is fluid overloaded

-medications support BP, glucose control, and symptom management, but they do not reverse all kidney dmg

renal replacement therapy

peritoneal dialysis, hemodialysis and CRRT

-peritoneal dialysis = uses peritoneal membrane as the filter, dialysate is infused into abdomen, allowed to dwell, then drained, removes waste and fluid by diffusion and osmosis, often done at home. RISK = peritonitis

-hemodialysis = blood is filtered through an external dialyzer (artificial kidney). required vascular access (AV fistula, graft, central catheter). usually 3x/ week for several hours. removes wastes, excess fluid and corrects electrolytes. RISK = hypotension

-CRRT = continuous renal replacement therapy used in critically ill/ unstable pt. slower continuous form of dialysis over 24 hours. better tolerated in pt with hemodynamic instability. Gradually removes fluid, solutes, and toxins

renal disorders

1.acute glomerulonephritis

2.nephrotic syndrome

3.nephrolithiasis

4.pyelonephritis

5.AKI and CKD synthesis

Acute Glomerulonephritis (AGN):

Definition, Epidemiology, & Etiology

*inflammation dmg the glomerulus and interferes with filtration, in many cases the process is triggered by an immune mechanism

-epidemiology = can be mild/ rapidly progressive. Can occur in kids and adults. untreated = chronic kidney dmg

-Etiology = poststreptococcal glomerulonephritis after streptococcal infection. acute rheumatic fever, autoimmune diseases such as lupus. certain infection including hep B/C and HIV

Acute glomerulonephritis (AGN)

pathophysiology

-an antigen-antibody reaction targets the glomerular membrane

-immune complexes deposit in the glomerulus and trigger inflammation

-the dmg filter allows blood cells and some protein to leak into the urine

-GFR declines, so urine output can fall and waste product accumulate

-decreased albumin in the bloodstream lower oncotic pressure and contributes to edema

Acute Glomerulonephritis (AGN):

Clinical Presentation, Diagnostics, & Treatment

-clinical presentation = hematuria, oliguria, edema, HPT, possible CVA tenderness, malaise, weakness, abdominal pain

-diagnostics = urinalysis: blood and protein. elevated BUN and creatine, possible low serum albumin, biopsy is the gold standard

-treatment themes = treat the cause when identifiable (ex: infection related disease). control edema and BP, use dietary restriction when ordered

Nephrotic Syndrome:

Core Pathophysiology

-glomerular dmg increases permeability of the filtration membrane, large amount of protein are lost into the urine, serum albumin falls, lower plasma oncotic pressure, fluid shifts form the vascular space into tissues, causing edema, associated with hyperlipidemia and sometimes HPT

Nephrotic Syndrome:

Presentation, Diagnosis, Treatment, & Complications

-manifestations = peripheral and facial edema. possible pleural effusion or ascites, heavy proteinuria, fatigue and reduced intravascular volume

-diagnostics = urinalysis is high protein. low serum albumin. elevated lipids may appear. renal ultrasound/ biopsy when needed to define cause

-management of complications = sodium and fluid restriction may be needed. diuretics help with edema in selected pt. ongoing protein loss increase risk for thrombosis and progression of kidney disease

Nephrolithiasis:

Epidemiology & Predisposing Factors

-kidney stones are common in adults and recurrence is frequent after 1st one

-geography, dehydration, dietary habits, and certain metabolic states as contributors

-low urine volume is a major modifiable risk factor

Nephrolithiasis:

Stone Types & Pathophysiology

Common Stone Types

-Calcium stones: often calcium oxalate

-Struvite stones: associated with infection

-Uric acid stones

-Cystine stones]

Pathophysiology Themes

-Crystals form when urine becomes supersaturated

-Urine pH, concentration, infection, and heredity all matter

-A stone may obstruct the ureter and lead to hydronephrosis and tissue injury

Nephrolithiasis:

Presentation, Diagnostics, and Management

-flank pain may radiate to the groin and often comes in waves

-hematuria and crystalluria are classic clues

-pt should strain urine when passing a stone so composition can be analyzed

-CT is the gold standard diagnostic test, ultrasound can also help

treatment: pain relief, hydration, selected procedures such as lithotripsy, ureteroscopy, prevention based on stone type,

Pyelonephritis:

Etiology & Pathophysiology

-usually caused by bacteria that ascend form the lower urinary tract

-women are affected more often because of shorter urethral length

-urinary obstruction instrumentation, and vesicoureteral reflux increase risk

-infection can become chronic when reflux or structural problems persist

Pyelonephritis:

Clinical Presentation & Nursing Focus

-fever, chills, flank pain, CVA tenderness, nausea/ V, dysuria or frequency

-chronic/ recurrent concerns = recurrent infection can scar renal tissue, function may decline over time, polyuria, nocturia, and proteinuria may appear in chronic disease

-nursing focus = monitor temperature, pain, and hydration, watch the urine and culture results, ask about obstruction, reflux, or prior UTI history

Chronic Kidney Disease:

Progressive Loss of Function

-CKD reflects gradual nephron loss over months to years

-as filtration declines, fluid, electrolyte, acid-base, endocrine, and waste-removal functions all deteriorate

-common complication include anemia, bone/ mineral imbalance. hypertension, and eventual ESRD

-CKD is not just low GFR - it is a multisystem disorder that changes assessment, medication safety, nutrition, and long term patient teaching.

AKI vs CKD

final comparison

AKI = hours to days. related to perfusion loss, nephron injury, or obstruction. may be reversible is treated fast. urine output may drop suddenly. rapid changes in BUN, creatine, and fluid status

-CKD = months to years. progressive nephron loss, usually not fully reversible, complications build over time across many body systems, may progress to ESRD and dialysis dependence

Summary of renal disorders

Kidney function: Filter blood, Balance fluids and electrolytes, Maintain pH, Support BP, RBCs, and vitamin D

-AKI = abrupt

-CKD = chronic

-Glomerulonephritis = inflamed filter

-Nephrotic syndrome = leaky protein-losing filter