What is renal failure?

Renal failure refers to temporary or permanent damage to the kidneys that results in loss of
normal kidney function. There are two different types of renal failure--acute and chronic. Acute
renal failure has an abrupt onset and is potentially reversible. Chronic renal failure progresses
slowly over at least three months and can lead to permanent renal failure. The causes, symptoms,
treatments, and outcomes of acute and chronic are different.
Diabetic nephropathy
- Diabetes can cause permanent changes, leading to kidney damage.

What is end-stage renal disease (ESRD)?

End-stage renal disease is when the kidneys permanently fail to work.

What are the symptoms of renal failure?

The symptoms for acute and chronic renal failure may be different. The following are the most
common symptoms of acute and chronic renal failure. However, each individual may experience
symptoms differently. Symptoms may include:
Poor appetite

Urinary incontinence

Pale skin

Bad breath

Hearing deficit

Detectable abdominal mass

Tissue swelling

Irritability

Poor muscle tone

Change in mental alertness

Metallic taste in mouth

Vomiting

Bone pain

Headache

Insomnia

Itching

Dry skin

Malaise

Fatigue with light activity

Muscle cramps

High urine output or no urine output

Recurrent urinary tract infections

Pathophysiology
Chronic renal failure often progresses through four stages.
1. reduced renal reserve shows a glomerular filtration rate (gfr) of 35% to 50% of normal;
2. renal insufficiency, a gfr of 20% to 35% of normal;
3. renal failure, a gfr of 20% to 25% of normal;

4. end-stage renal disease, a gfr less than 20% of normal.

"Nephron damage is progressive; damaged nephrons can't function and don't recover. The
kidneys can maintain relatively normal function until about 75% of the nephrons are
nonfunctional. Surviving nephrons hypertrophy and increase their rate of filtration, reabsorption,
and secretion. Compensatory excretion continues as gfr diminishes.
Urine may contain abnormal amounts of protein, red blood cells (rbcs) and white blood cells or
casts. The major end products of excretion remain essentially normal, and nephron loss becomes
significant. As gfr decreases, plasma creatinine levels increase proportionately without regulatory
adjustment. As sodium delivery to the nephron increases, less is reabsorbed, and sodium deficits
and volume depletion follow. The kidney becomes incapable of concentrating and diluting urine.
If tubular interstitial disease is the cause of chronic renal failure, primary damage to the tubules-the medullary portion of the nephron--precedes failure, as do such problems as renal tubular
acidosis, salt wasting, and difficulty diluting and concentrating urine. If vascular or glomerular
damage is the primary cause, proteinuria, hematuria, and nephrotic syndrome are more
prominent.
Changes in acid-base balance affect phosphorus and calcium balance. Renal phosphate excretion
and 1,25(oh)2 vitamin d3 synthesis are diminished. Hypocalcemia results in secondary
hypoparathyroidism, diminished gfr, and progressive hyperphosphatemia, hypocalcemia, and
dissolution of bone. In early renal insufficiency, acid excretion and phosphate reabsorption
increase to maintain normal ph. When gfr decreases by 30% to 40%, progressive metabolic
acidosis ensues and tubular secretion of potassium increases. Total-body potassium levels may
increase to life-threatening levels requiring dialysis.
In glomerulosclerosis, distortion of filtration slits and erosion of the glomerular epithelial cells
lead to increased fluid transport across the glomerular wall. Large proteins traverse the slits but
become trapped in glomerular basement membranes, obstructing the glomerular capillaries.
Epithelial and endothelial injury causes poteinuria. Mesangial-cell proliferation, increased
production of extracellular matrix, and intraglomerular coagulation cause the sclerosis.
Tubulointerstitial injury occurs from toxic or ischemic tubular damage, as with acute tubular
necrosis. Debris and calcium deposits obstruct the tubules. The resulting defective tubular
transport is associated with interstitial edema, leukocyte infiltration, and tubular necrosis.
Vascular injury causes diffuse or focal ischemia of renal parenchyma, associated with thickening,
fibrosis, or focal lesions of renal blood vessels. Decreased blood flow then leads to tubular
atrophy, interstitial fibrosis, and functional disruption of glomerular filtration, medullary
gradients, and concentration.
The structural changes trigger an inflammatory response. Fibrin deposits begin to form around
the interstitium. Microaneurysms result from vascular wall damage and increased pressure
secondary to obstruction or hypertension. Eventual loss of the nephron triggers compensatory
hyperfunction of uninjured nephrons, which initiates a positive-feedback loop of increasing
vulnerability.
Eventually, the healthy glomeruli are so overburdened that they become sclerotic, stiff, and
necrotic. Toxins accumulate and potentially fatal changes ensure in all major organ systems.