Chronic Kidney Disease: How to avoid the disease

 Chronic Kidney Disease: How to avoid the disease, what is the treatment?

Chronic kidney disease, also known as chronic renal failure, is a term that includes all degrees of decreased kidney function from damage at risk through mild, moderate or severe kidney injury. CKD is a worldwide public health problem, which carries a relatively poor prognosis. It is more prevalent in the elderly population.

Kidney disease in younger people

• However, younger people and children may also experience progressive chronic kidney disease. According to the reports of kidney disease being the tenth leading cause of death around the world, CKD is associated with an increased risk of cardiovascular disease and end-stage renal disease. The Kidney Disease Outcomes Quality Initiative, or KADOKAWA of the National Kidney Foundation of the United States, established a definition and classification for CKD in 2002.

• According to this, CKD is defined as kidney damage or a decreased GFR of less than 60 millilitres per minute for one point seventy-three square meters, which is the average body surface area of a normal adult for at least three months.

• According to the above-mentioned classification, the stages of KDDI are as follows stage one, kidney damage with normal or increased GFR typically more than 90 millilitres per minute for one point seventy-three square meters.

Chronic Kidney disease stages

• Stage two mild reduction in GFR, typically between 60 to 89. Stage three, a moderate reduction in GFR, typically between 45 to 59. Stage three B moderate reduction in GFR, typically between 30 to 44 stages for a severe reduction in GFR, typically between 15 to 29 and stage five. Severe reduction in GFR, typically less than 15 millilitres per minute per one point seven three square meters or dialysis. However, measurement of GFR alone may not be sufficient to identify the stage one and two of KDDI.

• In such cases, the presence of one or more of the following markers of kidney damage can establish the diagnosis of albumin area of more than 30 milligrams per day, or an albumin creatinine ratio of more than 30 urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, histological abnormalities, structural abnormalities detected by imaging studies and history of kidney transplantation. 

Chronic Kidney disease causes

• Now let's discuss the causes and pathophysiology of chronic kidney disease. A normal kidney contains approximately one million nephrons, each of which contributes to the total glomerular filtration rate regardless of the cause. The ultimate factor, which leads to CKD is kidney injury, which causes irreversible loss of functional nephrons. 

• The most common cause for this kidney injury in CKD is diabetic nephropathy. Although the exact cause of diabetic nephropathy is unknown, three main pathological manifestations are thought to be the cause for the development of diabetic nephropathy, including hypoglycemia, which causes hyperfiltration followed by renal injury, formation and deposition of advanced glycation end products in various parts of the kidneys, including glomerular vessels, glomerular basement membrane and extracellular matrix of the nephron, and increased production of cytokines such as Interleukin one and tumour necrosis factor-alpha and growth factors such as transforming growth factor-beta and vascular endothelial growth factor.

Chronic Kidney disease causes

• These pathologies lead to three main histological changes in the nephrons thickening of the glomerular basement membrane Masingill expansion and glomerular sclerosis, which may result in irreversible loss of nephrons. Another main cause of CKD is hypertension. Persistent hypertension causes thickening of arterial walls, in this case, the renal arteries. 

• And this will lead to less blood supply to the kidneys, which in turn will cause activation of the renin-angiotensin-aldosterone system and further increase the blood pressure. This will cause more thickening of arterial walls and lead to ischemic necrosis of the nephrons.

• Unrecovered acute renal failure is another cause. Acute renal failure is reversible. However, if not corrected, it can lead to chronic kidney disease. There are many causes for acute renal failure. Find the causes for acute renal failure and make a list as of today's homework. Another cause for KDDI is vascular diseases, including renal artery stenosis Atheros Embla and thromboembolic hypertensive neuro sclerosis vasculitis and renal vein thrombosis. 

• Glomerular diseases also can cause irreversible nephron loss and lead to chronic kidney disease. Common glomerular diseases include the following membranous nephropathy, Allport syndrome, IGA nephropathy, minimal change, disease focal and segmental glomerular sclerosis, membranous proliferative glomerulonephritis and rapidly progressive glomerulonephritis.

Chronic Kidney disease pathophysiology

• In addition, cystic kidney disease, tubular, interstitial diseases, urinary tract obstruction or dysfunction. Recurrent kidney stone disease and congenital defects of the kidney and bladder can cause irreversible nephron loss and lead to chronic kidney disease. Almost all the above-mentioned causes are primary causes of CKD. In addition to those, there are secondary causes for CKD as well.

• These include systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disorder, scleroderma, hepatitis B and C infection, syphilis, HIV infection and parasitic infections.

Chronic Kidney disease clinical presentation

• As mentioned earlier, regardless of the underlying ideology, the main factor that leads to CKD is irreversible nephron loss. However, despite the progressive destruction of nephrons, the kidney has an innate ability to maintain GFR through compensatory hypertrophy of the remaining healthy nephrons and glomerular hyperfiltration. This nephron adaptability allows for continued normal clearance of plasma solutes. Therefore, plasma levels of substances such as Urea and creatinine start to show measurable increases only after the total GFR has decreased from about 50 per cent of the normal value.

1. The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive renal dysfunction. The increased glomerular capillary pressure may damage the capillaries leading initially to secondary focal and segmental glomerular sclerosis and eventually to global glomerulosclerosis, which causes a gradual decrease in GFR. Now let's discuss the clinical manifestations of chronic kidney disease patients with CKD stages one to three are frequently asymptomatic. These people do not experience clinically evident disturbances in water and electrolyte balance or metabolic or endocrine functions.

Chronic Kidney disease diagnosis

• Generally, these disturbances become clinically evident in stage four and five of CKD. However, patients with tubules, interstitial diseases, cystic diseases and nephrotic syndrome may experience symptoms like Polli Uria hematuria and oedema during the early stages of KDDI. One of the major clinical consequences of KDDI is sodium and water handling abnormalities. 

• This generally becomes clinically manifested when the GFR falls less than 10 to 15 millilitres per minute for one point seventy-three square meters. Failure of sodium and water excretion leads to sodium and water retention, followed by extracellular fluid volume expansion and total body volume overload.

• As kidney function declines, further, sodium retention and extracellular fluid volume expansion lead to peripheral oedema, pulmonary oedema and hypertension tubules. Interstitial renal diseases represent the minority of cases of KDDI.

• However, it is important to note that such diseases often cause fluid loss rather than overload. Thus, despite moderate or severe reductions in GFR, tubulointerstitial renal diseases may manifest first as poor urea and volume depletion with the inability to concentrate the urine. 

• Another manifestation of CD is hyperkalemia, the ability to maintain potassium excretion at near-normal levels is generally maintained in CKD. As long as aldosterone secretion and Destil flow are maintained, hyperkalemia usually does not develop until the GFR falls to less than 20 to 25 millilitres per minute for one point seventy-three square meters.

Chronic Kidney disease treatment

• If you can remember your physiology, knowledge of aldosterone is a hormone that increases the expression of potassium ions in urine in exchange for sodium. It primarily acts on the principal cells of the collecting tubules to increase the uptake of sodium into the blood in exchange for potassium through the sodium-potassium pump. 

• As you can see in this picture, this concentrates sodium-potassium sodium from the tubular lumen to the blood in the Peritubular capillaries. Potassium ions, which are being pushed into the principal cells, are excreted via urine.

• How does aldosterone activate specific genes in the nucleus and cause the expression of sodium, potassium pumps, sodium channels in the luminal membrane and enzymes required to increase the sodium uptake? However, during the late stages of KDDI, aldosterone secretion is reduced due to the reduced renin secretion by the kidneys. This causes retention of potassium in the.