- interference of flow of urine along urinary tract

- obstruction

- impedes flow

- dilates the urinary system proximal to the obstruction

- increases the risk for infection

- caused by

- kidney stones

- compression fr. a tumour or inflammation

- obstruction due to anatomic changes in the urinary system

- caused by kidney stones, tumours, inflammation

- occur in the ureter or within the kidney (pelvis) or nephron

- kidney stones

- tumours

- inflammation

- dilation and fibrosis occur first at the distal nephron (7d)

- then the proximal nephron (14d)

- by 28 d, the glomeruli have been damaged, and the cortex and medulla are reduced in size

- irreversible damage can occur if the obstruction remains for 4 weeks

- however, partially recovery can occur if the blockage is removed w/in 56 to 69 d

- if one kidney is obstructed, the body can compensate:

- in the unobstructed kidney, the glomeruli and tubules are increased in size but not the total # of functioning nephrons

- this way the unobstructed kidney can make up for the reduction in fxn of the obstructed kidney

- this ability decreases w/ age and the process is reversible if obstructed kidney recovers

- kidney stones

- can be formed of crystals, proteins or other substances

- influenced by factors including age, fluid intake, and diet

- composed of calcium oxalate or phosphate (70-80%), due to factors including high urine calcium

- located in the kidneys, ureters and urinary bladder

- due to factors including high urine calcium

- caused by

- hyperabsorption of calcium fr. the intestines

- hyperparathyroidism

Renal Colic

clinical manifestation of kidney stones

- moderate to severe pain (can be incapacitating, w/ nausea)

- it can indicate where the obstruction is in the ureter

- eg. originating of renal pelvis or proximal ureter vs radiating to the lower abdomen (midureter)

- removing stones

- managing pain

- reduction of further formation through increasing fluid flow and altering diet

- primarily related to storage of urine in the bladder or emptying of urine thru the bladder outlet

- can be caused by 

- neurogenic bladder

- physical obstruction

- bladder dysfxn caused by neurologic disorders

- dysfxn (incontinence/fxnl obstruction) depends on where the damage has occured in the nervous system

- scarring of the urethra (infection, surgery)

- enlarged prostate

- inflammation of glomerulus

- caused by immunologic responses, infection, diabetes mellitus, etc.

1. Type III

- deposition of circulating Ab/Ag complexes into the glomerulus

2. Type II

- Ab reacting agsnt Ag w/in the glomerulus

- Ab activate complement proteins w/c summon macrophages and neutrophils

- macrophages and neutrophils secrete compnds that damage the glomerular cells 

- this increases membrane permeability w/c allow proteins and RBS to escape into filtrate

- proteinuria and/or hematuria develop

- nephrosis

- excretion of 3.5g or more of protein/day in urine

- characteristic of glomerular injury

- due to certain forms of glomerulonephritis, vascular disorders, diabetes mellitus, etc.

- excretion of blood cells in addition to protein (not as much protein as in nephrosis)

- due to alterations in glomerulus 

- due to inflammation

- blood urea nitrogen

- concentration of urea in the blood

state of kidney:

- reflects glomerular filtration

- b/c urea is filtered at the glomerulus, as filtration drops, BUN rises

- also reflects urine-concentrating capacity

- b/c urea is reabsorbed fr. the nephron, if flow thru nephron decreases (due to dehydration or renal failure, BUN rises)

- creatinine is produced by the muscles, and it is filtered at the glomerulus and never reabsorbed

- b/c of this, it indicates the amount of filtration that is occuring at the glomerulus

- if glomerular filtration rate decreases, the plasma creatinine concentration increases and vice versa

- acute kidney injury

- sudden decline in kidney fxn w/a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood (increased BUN and plasma creatinine)

- risk - injury - failure - loss - end stage disease

- its a criteria for acute kidney injury based on glomerular filtration rate and urine output

1. prerenal acute kidney injury

- most common reason for AKI

2. intrarenal acute kidney injury

3. postrenal acute kidney injury

- the decrease in GFR is caused by renal hypoperfusion

- lower hypoperfusion may be due to:

- renal vasoconstriction

- hypotension

- hypovolemia

- hemorrhage or inadequate cardiac output

- if pressure continues to be low, lack of oxygen delivery can cause cell injury and necrosis

- usually results fr. tubular necrosis as a result of occurences including:

- prerenal injury

- ischemia after surgery

- exposure to toxins eg. carbon tetrachloride

- glomerulonephritis

- vascular disease (DIC)

- allograft rejection

- tumor growth

- urinary tract obstructive disorders

- rare, usually occurs w/ urinary tract obstruction that affects both kidneys eg. neurogenic bladder

- causes an increase in pressure upstream, resulting in decreased GFR

1. Initiation - reduced perfusion or toxicity in w/c the kidney injury is evolving; possible to reverse

2. Maintenance - kidney injury has been established - dysfxn may last fr. weeks to months

- urine output is the lowest

- serum creatinine and BUN levels both increase

3. Recovery - interval when kidney injury is repaired - normal renal fxns occurs

- low output of urine

- begins w/in 1 day after a hypotensive event and lasts 1-3 weeks, depending upon the duration of ischemia/severity of injury

- may not occur w/ some AKI (nephrotoxins one) but plasma creatinine and BUN levels will increase

- primary goal is to maintain life until renal fxn has been recovered

- correct fluid and electrolyte imbalances

- treat infections

- maintain nutrition

- drugs and metabolites are not excreted

- continuous renal replacement therapy eg. dialysis, kidney transplant may be required

Chronic Kidney Disease

(CKD)

- declining GFR

- a progressive loss of renal fxn

- chronic renal failure, renal insufficiency

- associated w/ systemic disease such as:

- hypertension

- diabetes mellitus

- chronic glomerulonephritis

- obstructive uropathies

- the unaffected nephrons are capable of hypertrophy and hyperfxn in their rates of filtration, reabsorption and secretion, in order to make up for the declining GFR

How does the urine of a person with CKD compare to that of a person with normally functioning kidney?

- they contain abnormal amounts of protein and blood cells

- the major end products are similar to normal fxning kidneys until advanced stages of renal failure - when there's a large loss of fxning nephrons

- increased levels of serum urea and other nitrogenous compnds related to decreasing kidney fxn

Uremic syndrome

(uremia)

- the systemic symptoms associated w/the accumulation of nitrogenous wastes and toxins in the plasma

- azotemia

- uremic syndrome (uremia)

1. sodium - kidney loses its ability to regulate sodium & H2O

- both are retained, contributing to edema

2. potassium - not secreted sufficiently in later stages

- can increase to  life-threatening levels

3. creatinine & urea - increase in the plasma as GFR decreases

4. pH - metabolic acidosis - decreased secretion of H+ and reabsorption of bicarbonate ions of the kidneys

5. calcium - less calcium is absorbed fr. the GIT (why?)

- this is detected by the parathyroid gland, w/c then increases levels of PTH w/c results in loss of calcium fr. the bone, increasing the risk of bone fracture

6. proteins & fat - advanced CKD causes decreases in amnt of proteins (loss of muscle mass & serum proteins); also a shift in the ratio of LDL/HDL, w/ more LDL causing increased atherosclerosis

- a general accumulation of fluid in body cavities and tissues

1. cardiovascular system

- major cause of death in CKD

- excess Na+ and H2O lead to hypertension

- excess LDL leads to increased atherosclerosis

- kidney produces less erythropoetin, so anemia may result, increasing cardiac workload

2. pulmonary system

- fluid overload

- acidosis results in Kussmaul respirations

3. hematologic system

- anemia, impaired platelet fxn

4. immune system

- overall suppression

5. neurologic system

- headache, pain, drowsiness, impaired conc. and memory loss - w/ later stages, seizures and coma

6. gastrointestinal system

- anorexia, vomiting constipation or diarrhea

7. endocrine and reproductive systems

- decrease in levels of sex steroids bring symptoms such as impotence, amenorrhea

- insulin resistance can occur as well as alterations in thyroid hormone metabolism

- elevated serum creatinine and BUN levels

- protein in the urine, particularly albumin

- confirmed by renal biopsy

- management includes dietary control to replace/restrict appropriate factors

- drugs to treat hypertension

- dialysis and renal transplantation