Kidney Disease

Kidney disease occurs when kidney function declines, disrupting the regulation of fluids, electrolytes waste products and acid base balance, acute kidney injury or AK I is a sudden decline in kidney function that's typically reversible.

Whereas chronic kidney disease or CKD is kidney damage, that is gradual and irreversible. Now, the kidneys are the body's natural blood filter.

They regulate what's in the blood, clearing it of metabolic waste and toxins and excreting them through urine. They're essential in regulating fluids and electrolytes, maintaining acid base balance, secreting hormones, essential for regulating BP and stimulating the production of red blood cells and activating Vitamin D within each kidney.

There are millions of tiny functional units called nephrons which consist of a renal corpuscle and renal tubules. The renal corpuscle is where blood filtration occurs and it includes a tiny bundle of capillaries called the glomerulus and the glomerular capsule or Bowman's capsule, which is a cup shaped structure that surrounds the glomerulus as blood flows through the glomerulus, an ultra filtrate of blood is created which is then collected by Bowman's capsule.

Then as it moves into the renal tubules, the filtrate is modified according to the body's needs and urine is produced in which waste is eliminated.

The rate at which filtration takes place is called glomerular filtration rate or GFR for short. And it's one of the main measures of kidney function.

Now, there are three different mechanisms that can cause kidney injury. First, prerenal kidney injury can occur when there's decreased blood flow to the kidneys.

Like from dehydration, hemorrhage or shock in certain individuals. Medications like non steroidal anti inflammatory drugs or nsaids.

Angiotensin converting enzyme or ace inhibitors or angiotensin receptor blockers. Or Arbs can also cause prerenal kidney injury by altering the normal autoregulation of blood flow within the kidneys.

Next, intrinsic or intrarenal kidney injury occurs when there's an ischemic or toxic insult that causes direct damage to the kidney tissue itself, including the tubules, glomeruli and renal blood vessels.

This can happen with nephrotoxic substances like certain medications such as vancomycin or cytotoxic chemotherapy agents or from ischemia, which can happen if either prerenal or postrenal kidney injury is prolonged.

Lastly, post renal kidney injury is caused when the normal outflow of urine from the kidneys is obstructed, which can happen with benign prostatic hyperplasia, renal calculi also called kidney stones and even when there is an obstructed or kinked indwelling urinary catheter.

Now, when it comes to CKD, it's most often caused by conditions such as hypertension and diabetes mellitus. Additionally, AK I can progress into CKD if the cause is not resolved.

Risk factors for both AK I and D include preexisting conditions that can affect normal kidney function, advanced age family history and exposure to potentially nephrotoxic substances.

All right. So the pathophysiology of AK I varies depending on the mechanism of injury.

In prerenal AK I, inadequate kidney perfusion leads to decreased G fr. The kidney's normal response to this low blood flow is to release renin, which activates the renin angiotensin aldosterone system or ras and antidiuretic hormone or A DH, which are aimed at raising BP, restoring renal perfusion and preserving GFR injury occurs if perfusion isn't restored.

Intrinsic AKI commonly involves damage to the renal tubules which triggers an inflammatory process that causes tubular epithelial cell damage in a patchy pattern of necrosis and apoptosis, dead and damaged cells slough off and accumulate in the lumen of the tubules and combine with inflammatory cells and proteins in the filtrate which then solidify into casts.

The casts cause obstruction of urine flow within the tubules and reduce GFR. They also increase intratubular pressure and damage tubular epithelial cells disrupting the tight junctions between them.

This leads to a breakdown of the blood urine barrier, causing a tubular back leak or a fluid that's already been filtered, leaks back into the bloodstream instead of being excreted in the urine.

Meanwhile, sustained renal vascular resistance leads to further intrarenal damage. Lastly, in postrenal AK I obstruction of urine flow from the kidney increases pressure within the tubules which then lowers the amount of fluid that's filtered decreasing G fr, no matter what the cause, decreased G FR results in decreased urine output.

And since less blood is being filtered, that means less waste products like nitrogen containing compounds in the blood such as urea and creatinine are filtered out.

So more stays in the blood resulting in a condition called azotemia. Now, clinical manifestations of AK I occur in three phases.

Prodromal oliguric and post oliguric during the prodromal phase. The injury is just starting and there's typically a normal to slightly decreased urine output as the GFR decreases serum B un and creatinine levels begin to rise.

Next. The oliguric phase is characterized by oliguria or low urine output.

In severe cases, Anura or in absence of urine production can occur or the kidneys stop producing urine altogether. This can lead to hypervolemia, edema, weight gain, hypertension and pulmonary crackles.

Serum electrolyte balance is disrupted, leading to the possibility of arrhythmias related to hyperkalaemia as the kidneys lose their ability to excrete hydrogen ions and reabsorb bicarbonate.

Metabolic acidosis may also be present. Azotemia can manifest as anorexia, nausea, vomiting, weakness and altered mental status.

Urinalysis may reveal a decreasing urine specific gravity, reflecting impaired tubular function and protein urea reflecting glomerular damage.

Creatinine clearance is often decreased, reflecting the kidney's impaired ability to clear creatinine from the bloodstream urine microscopy will often reveal red blood cell white blood cell or tubular epithelial casts.

The post oliguric phase begins as the kidneys start to recover polyurea or increased urine output occurs as glomerular function resumes but the damaged tubules aren't yet ready to effectively concentrate urine.

This can lead to fluid volume deficit and low serum levels of electrolytes like sodium and potassium. Now, as far as CKD goes, progression is monitored using a five stage system based on the G FR.

It ranges from stage one where kidney damage is present. The GFR is within a normal range and the patient is asymptomatic to stage five, which represents a markedly decreased GFR and end stage kidney disease.

The impaired kidney function and accumulation of toxins affects nearly every organ system. For instance, neurological symptoms can include uremic encephalopathy, manifesting as confusion, agitation and peripheral symptoms like pain, numbness and tingling, renal osteodystrophy caused by alterations in calcium phosphate, magnesium and Vitamin D metabolism.

Manifesting as bone pain and an increased fracture risk, fluid overload, which can lead to pulmonary edema and heart failure and decreased erythropoietin production which can lead to anemia.

All right. As a quick recap, kidney disease occurs when kidney function declines, disrupting the regulation of fluids, electrolytes waste products and acid base balance.

AK I is a sudden decline in kidney function that's typically reversible. Whereas CKD is gradual and causes irreversible kidney damage.

AK I can be categorized as prerenal, intrinsic or postrenal and can progress to D if left untreated. Clinical manifestations of AK I occur in three phases.

Prodromal, oliguric and post oliguric CKD can affect nearly every organ system.