Renal Failure and Acute Kidney Injury

Reduced blood flow to kidneys due to lowered blood volume (e.g., hemorrhage), distributive shock, or vasoactive drugs.

Decreased urine output, higher BUN/creatinine ratio (e.g., 15:1 to 20:1 instead of 10:1).

Damage to the kidney's structures (glomerulus, tubules, etc.).

Drugs like aminoglycosides and certain chemotherapy drugs damaging the kidney tubules.

Myoglobin, hemoglobin, excess uric acid or proteins block the kidney tubules.

Initiation, maintenance (declining function), and recovery (improving function).

Obstruction of urine flow from the kidneys.

Sudden drop in GFR and increased serum creatinine.

Correcting underlying cause, preventing infections, potentially dialysis.

Progressive loss of kidney function (GFR) over months or years.

Remaining healthy nephrons enlarge to try to meet the body's needs.

Decreased renal reserve, renal insufficiency, and uremia (end-stage).

Isosthenuria (urine isotonic with blood) causing hyponatremia initially.

Fluid and ion retention, potentially leading to heart failure and edema. Also includes things like hyperkalemia and metabolic acidosis.

Decreased calcitriol, low calcium, and high parathyroid hormone (PTH) leading to bone problems.

High phosphate levels due to impaired kidney excretion.

Bone problems from mineral imbalances (calcium, phosphorus).

Reduced red blood cell production due to lower erythropoietin (EPO) levels.

High blood pressure due to fluid retention, needing treatment to slow disease progression.

Problems with brain function due to waste buildup, leading to reduced awareness.

Slow disease progression, consider dialysis/transplantation, diet management.

Glomerular filtration rate: measure of how well kidneys filter blood.

Serum creatinine is a useful measure of GFR but is not perfect.

Vasoconstrictors, such as certain medications or mediators, reduce renal blood flow by causing blood vessels in the kidneys to narrow, leading to hypoperfusion.

A decrease in GFR (glomerular filtration rate) leads to reduced urine output because the kidneys are filtering less blood, resulting in less urine production.

A normal ratio is 10:1, indicating the kidneys are functioning properly.

The ratio rises to 15:1 to 20:1 in prerenal failure due to the kidneys' inability to filter waste products efficiently.

Prerenal injury is characterized by a significant decrease in renal blood flow, usually due to factors like hypovolemia, shock, or medications.

NSAIDs can worsen hypoperfusion by preventing blood vessel dilation in the kidneys, leading to reduced blood flow.

These medications reduce the effects of renin, a substance that increases vasoconstriction, thereby aiding in maintaining renal perfusion.

Tubular epithelial cells are susceptible to ischemia (lack of blood flow) and toxins, which can trigger inflammation and fibrosis in the kidneys.

Intrinsic AKI is caused by damage to the kidney's structures, like the glomerulus, tubules, or interstitial cells. This damage can be caused by various factors, including acute tubular necrosis, nephrotoxic drugs, tubular obstruction, and infection.

Acute tubular necrosis is a major cause of intrinsic kidney injury. It occurs when the kidney's tubules, which are responsible for filtering waste and reabsorbing water and nutrients, are damaged.

Prerenal injury (reduced blood flow to the kidneys) can eventually lead to intrinsic kidney injury, causing damage to the tubules and glomerulus.

Some drugs are toxic to the kidneys, especially the proximal convoluted tubule (PCT). These drugs can damage the tubules, leading to intrinsic AKI.

Intratubular obstruction occurs when substances like myoglobin, hemoglobin, uric acid, or myeloma light chains block the tubules, hindering the flow of urine.

Myoglobin, a muscle protein, can be found in the urine after muscle trauma like rhabdomyolysis. It can contribute to an intratubular obstruction.

Chemotherapy drugs accumulate in the PCT, leading to direct damage to the tubular cells and endothelial cells. They can cause DNA damage.

AKI causes a decrease in glomerular filtration rate (GFR), meaning the kidneys are unable to filter blood effectively.

The maintenance phase of AKI features a marked decrease in GFR, leading to the retention of toxic metabolites such as potassium and nitrogenous wastes. These retained metabolites can cause fluid retention (edema, water toxicity, and pulmonary congestion) and hypertension. Hyperkalemia can also occur.

The recovery phase of AKI is characterized by an increasing urine output, and a gradual decrease in serum creatinine, potassium, and BUN levels. However, it can take some time for these levels to completely normalize.

Chronic kidney disease can progress without noticeable symptoms until about half of the nephrons are lost. This is typically in stage 4 or 5 of CKD.

Progressive loss of kidney function characterized by a slow decline in GFR over months or years.

As nephrons die in CKD, the kidneys struggle to filter waste and excess fluids, leading to fluid and electrolyte imbalances. This can cause swelling (edema) and worsen heart conditions.

Impaired kidney function leads to reduced potassium excretion, causing elevated potassium levels in the blood (hyperkalemia).

CKD affects the kidneys' ability to properly regulate acid-base balance, potentially leading to metabolic acidosis.

CKD reduces calcitriol (vitamin D) production, leading to decreased calcium absorption and increased calcium loss in urine, causing low blood calcium levels.

Low blood calcium levels stimulate the parathyroid glands to release more parathyroid hormone (PTH), aiming to increase calcium levels. This can lead to bone problems.

Reduced kidney function leads to increased phosphate levels in the blood, as the kidneys cannot filter it out effectively.

Mineral imbalances (calcium, phosphate) in CKD disrupt bone remodeling, weakening bones and leading to decreased bone density.

CKD progresses through stages defined by GFR levels. Early stages involve a decrease in renal reserve, followed by renal insufficiency, and finally, uremia in end-stage disease.

In the early stages, osmotic diuresis occurs, leading to large volumes of concentrated urine. Patients may experience hyponatremia and azotemia.

Azotemia worsens to uremia, leading to fluid and waste retention. Hypervolemia, hyperkalemia, hyperphosphatemia, and metabolic acidosis develop.

High blood pressure increases glomerular filtration, leading to proteinuria and damaging the glomerulus, hastening CKD progression.

ACE inhibitors dilate the efferent arterioles, reducing glomerular pressure and proteinuria.

Dietary management in CKD varies based on the stage of the disease. In early stages, fluid and sodium need to be replenished. In later stages, fluid intake must be restricted, and electrolytes managed.

Protein restriction in CKD helps decrease the workload on the kidneys, reducing waste products and preventing further damage.

The dialysate solution is adjusted to remove or replace substances depending on their concentration in the blood. Potassium and wastes are hypotonic to facilitate removal, while bicarbonate may be hypertonic to treat acidosis.

Chronic kidney disease (CKD) is a progressive loss of kidney function over time. It's like a slow leak in your kidneys.

In early CKD, your kidneys can still compensate. It's like your healthy nephrons (filtration units) are working overtime.

Late CKD is when your kidneys are struggling to function. It's like your kidneys are overwhelmed with waste.

Azotemia is the build-up of nitrogenous waste products in the blood. It's like your body is holding onto too much garbage.

Uremia is a serious complication of CKD where waste products build-up to dangerous levels. It's like your body is drowning in garbage.

CKD symptoms can include fatigue, swelling, decreased urine output, and loss of appetite. They often appear when kidney function is significantly compromised.

CKD can lead to high blood pressure as kidneys struggle to regulate fluids. It's like your kidneys are having a hard time controlling the pressure in your system.

Diet is important in CKD to reduce stress on your kidneys. It's like eating a healthy diet to help your overworked kidneys.