Pathophysiology

Defined as kidney damage or a GFR less than 60mL/min for 3 monts or more. Represents a loss of functioning nephrons (decreased endocrine function, glomerular filtration, tubular reabsorption

Conditions that cause permanent loss of nehphrons e.g. diabetes, hypertension, glomerulonephritis, polycystic kidney disease

Symptos occur gradually and only if disease far advanced -> copensatory ability of kidney is high.
Reaining nephrons undergo structural and functional hypertrophy

High protein count in urin (GFR), or RBC's and WBC's in urine or abnormal findings on iaging studies

Accuulation of nitrogenous wastes: Urea and blood urea nitrogen accuulates in blood
Alteretions in water, electrolyte, acid base balance: dehydration (or opposite), sodium excretion
mineral and skeleteal disorders: Abnormalities of calcium and posphate metabolism
Anemia and coagulation disorders: Less vitain D syntehsis -> anemia
hypertension and alterations in cardiovascular function
GI disorders:
Neurological complications
Iunologic function disorders:

Nitrogenous waste accumulates in blood (Urea or Blood Urea nitrogen (BUN))

Uremia (urine in the blood) can occur which can lead to weakness and fatigue, vomitting, and confusion (up to death without dialysis or renal transplan)

Dehydration or fluid load, ability to concentrate urine is diinished -> polyuria (excessive urination).
Reduction in sodium excretion -> dehydration or fluid load

Increased potassium excretion in nephrons -> can result in hyperkalemia (too much potassium in blood)

Kidney regulate pH by reabsorption of bicarbonate and secretion of H+, with declined kidney function acidosis (increased acididty of blood) develops

Pospate excretion is reduced, calcium excretion is increased, thus low Ca serum levels -> parathyroid hormone release increases resorption of Ca from bones -> weak bones which could develop in bone disease.

Vitamin D synthesis also impaired (since kidney convert from inactive to active for) -> can lead to hyperthyroidism

Chronic anemia, because chronic blood loss, hemolysis (rupture of RBC's) and decreased erythropoietin -> decreased production of RBC's (due to loss of erythropoietin which stimulates that)

Group of kidney disorders characterized by fulid-filled scars/segents that originate from the tubular structure.

Autosoal dominant polycystic kidney disease (ADPKD): more comon
Autosomal recessive polycystic kidney disease (ARPKD): rare

Most forms are heditary. (Mutation of PKD1 and PKD2)

Not clear. Cysts arise in segents of renal tubules from epithelial cells. Cells have a high proliferation rate and defective basement membrane which allows for dilation and cyst (fluid flled sac) formation.

Total kidney volue used to measure cyst expansion and development

Asyptomatic initially. Later on pain due to enlarging cysts, hematuria (bleeding into cyst), cyst-infections, hypertension (compression of internal blood vessels and activation of renin angiotensin mechanism)

Kidneys usualle enlarged. External contour distorted by cysts. Can spread to liver, pancreas and spleen

dilation of cortical and medullary collecting tubules, but surface is smooth. More found in infants

Urine filled dilation of renal pelvis (urine collects here) and calices associated with kidney atrophy (reductio in size) due to obstruction of urine outflow

Obstructio affects outflow from distal ureter, increased pressure dilates ureter -> hydroureter

Depend on site of obstruction.
Can cause pain because of swelling or obstruction (e.g. kidney stones).
Partly obstruction destroys kidney due to slowed urine flow.

earlyest manifestation to obstruction is failure of kidney to concentrate urin -> exessive urination (polyurea)

Any level of urinary tract. Urethra to renal pelvis

Sudden or insidious, partial or coplete and unilateral or bilateral.

Short duration= acute, chronic if long-lasting

Bilateral obstruction causes acute renal failure.

Obstructed kidney undergoes atrophy (dies off)

kidney stones, pregnancy, tumors, bladder cancer, bladder stones, congenital deffects

Stasis of urine (retention) followed by infection and stone formation.
Progressive dilation of renal collectin ducts -> causes atrophy of renal tissue

Supersaturated urine (dehydration?), presence of a nucleus to form cristal, deficiency of inhibitors of stone formation

Pain! (when stretching the ureter e.g. by collecting water or swelling) Gets worse with drinking a lot

Skin may be cool and clammy, nausea and vomitting

Treatment of kidney failure, life sustaining when waiting for transplation.

Hemodialysis and Peritoneal dyalysis

Artificial kidney (blood delivery syste, diallyzer and fulid).

Dialyzer consists of capillary tubes, semipermeable (not to RBC and plasma proteins) for other blood coponents to flow along concentration gradient from blood to dialyzer fluid.

Substances that need replacement are added to the dialyzing solution

Thin serous mebrane, semipermeable (same purpose as in hemodialysis) is placed in peritoneal cavity.

Catheter allows filling with solution, which then stays in peritoneal cavity for some time an is drained at the end

Obstruction with retention or stasis of urine.
Incontinence: loss of urine involuntary due to structural changes of bladder/urethra or surrounding organs (but also neurologic control of bladder function)
Cancer

Acoording to cause (congenital or aquired), degree (partial or complete), level (upper or lower) and duration (acute or chronic)

Congenital obstructions or damage of specific nerves.

STI's and infections, bladder tumors, or other tumors compressing urinary tract. In males compression of urethra by prostate enlargement e.g.

Early stages: hypertrophy (increased volume) of bladder and hypersensitivity resulting in bladder spasm. urination urgency and incontinence. Build up of urine can lead to kidney damage and urinary tract infections.

Second stage: compensatroy mechanisms no longer effective (bladder too full?). frequent urination due to remaining urine in bladder (inomplete bladder empty feeling)

Being female (twice as often affected) and elderly.

Stress (sneezing, coughing,..), Overreactive bladder, urge incontinence (hyperactivity of detrusor muscle), overflow incontinence (pressure in bladder higher than detrusor activity) and functional incontinence (not able to feel/know that bladder is almost full).

It is derived from the transitional (urothelium) cells. Can for low-grade noninvasive up to high-grade invasive tumors which invade bladder wall.

Possibly carcinomas that are excreated in urine.

Caused by, paint, chemicals, petroleum, smoking but also chronic infections and bladder stones increase risk