renal failure is a condition in which the kidneys fail to remove metabolic end products from the blood and regulate fluid, electrolyte, and pH balance of the extracellular fluids
AKI is abrupt in onset and is often reversible if recognized early and treated appropriately
CKD is the end result if irreparable damage to the kidneys that develops slowly, usually over the course of a number of years
underlying causes of renal failure:
renal disease
systemic disease
urologic effects of non-renal origin
assessment measures to identify persons at risk for development of AKI includes those with preexisting renalinsufficiency and diabetes and elderly persons
aging has effects on one's renal reserve
prerenal causes of AKI:
hypovolemia
decreased vascular filling
heart failure and cardiogenic shock
decreased renalperfusion due to vasoactive mediators, drugs, and diagnostic agents
postrenal causes of AKI:
bilateralurethralobstruction
bladderoutletobstruction
both prerenal and postrenal causes of AKI will result in decreased GFR due to:
the result of a lack of flow to the kidney (prerenal)
result of backpressure on the kidney (postrenal)
acute tubular necrosis occurs due to:
prolonged renal ischemia
exposure to nephrotoxic drugs, metals, and organic solvents
trauma, burns, and major surgery are common precursors
intratubular obstruction resulting from hemoglobinuria, myoglobinuria, myeloma light chains, or uric acid casts
acute renal disease
the onset or initiating phase of AKI lasts hours or days and includes the time from the onset of the precipitating event until tubular injury occurs
the maintenance phase of AKI is characterized by a marked decrease in the GFR
the recovery phase of AKI is a period during which repair of renal tissue takes place
common causes of CKD:
hypertension
diabetes mellitus
polycystic kidney disease
obstructions of the urinary tract
glomerulonephritis
cancers
autoimmune disease
diseases of the heart or lungs
chronic use of pain medication
CKD is slow to develop and arises from other disorders
over time, the renal tissue is slowly damaged and lost in CKD, resulting in an insidious onset
Stage 1 CKD is kidney damage with normal or increased GFR
stage 2 CKD is kidney damage with mild decrease in GFR
stage 3a CKD is mild to moderate decrease in GFR
stage 3b CKD is moderate to severe decrease in GFR
stage 4 CKD is severe decrease in GFR
stage 5 CKD is kidney failure/ESRD
progression of CKD:
diminished renalreserve
renal insufficiency
renal failure
end-stagerenaldisease
clinical manifestations of CKD:
azotemia
alterations in water, electrolyte, and acid-base balance
mineral and skeletal disorders
anemia and coagulation disorders
hypertension and alterations in cardiovascular function
GI disorders
neurologic complications
disorders of skin integrity
immunologic disorders
factors determining manifestations of CKD:
the extend of renal function that is present
coexisting disease conditions
the type of renal replacement therapy that the person is receiving
in azotemia, urea starts to accumulate in the blood, which is an early sign of kidneyfailure
with CKD disease progression, azotemia can eventually result in uremia
azotemia is nitrogenous waste accumulation in the blood that can occur without symptoms
uremia is symptoms associated with decreased clearance of nitrogenous wastes
uremia occurs when approximately two-thirds of the nephrons are destroyed
causes of uremia:
encephalopathy
periphral neuropathies
pruritus and serositis
sodium and water balance helps the kidneys function in the regulation of ECF volume
sodium and water imbalance can be an early sign of kidney damage, causing isosthenirua or polyuria with nearly isotonic urine to plasma
in CKD, one has a reduced ability to excrete sodium which leads to fluid volume expansion, edema, and hypertension
approximately 90% of potassium excretion is through the kidneys
potassium excretion increases as they kidney adapts to a decrease in GFR
hyperkalemia can happen in late stage CKD and renal failure
the kidneys normally regulate blood pH by eliminating H+ produced in metabolic processes and regenerating bicarbonate
breakdown in the kidneys' ability to regulate blood pH can result in metabolic acidosis
metabolic acidosis can become stabilized with the buffering capacity of bone, but can result in skeletal disorders due to increased bone resorption