In: Nursing
Chronic Kidney Disease and diabetes patient
how it effect how long ?
what is recommendation patient?
How to prevent ?
What is the cause?
What is the pathophysiology?
This should be article for past 3 yeras
Diabetes is the leading cause of kidney failure, accounting for 44% percent of new cases. Current research suggests that control of high blood pressure is a key factor in slowing this disease. Strict control of blood sugar levels and reduction of dietary protein intake are also important. Treatment to prevent diabetic kidney disease should begin early — before kidney damage develops.
In the United States, over 29 million people have diabetes. Of these, 21.0 million are diagnosed and 8.1 million are undiagnosed.
QUESTION:-what is recommendation patient?
ANSWER:-there are the patients with multi speciatity disoreder . For example a parient with CLD should consult a Nephrologist meanwhile a patient with CKD and DM must consult both Nephrologist and an Endocrinologist .
Chronic kidney disease (CKD) is associated with insulin resistance and, in advanced CKD, decreased insulin degradation. The latter can lead to a marked decrease in insulin requirement or even the cessation of insulin therapy in patients with type 2 diabetes. Both of these abnormalities are at least partially reversed with the institution of dialysis. (See "Carbohydrate and insulin metabolism in chronic kidney disease".)
Because of the uncertainty in predicting insulin requirements, careful individualized therapy is essential among patients who have advanced CKD or are initiating dialysis.
The insulin requirement in any given patient depends upon the net balance between improving tissue sensitivity and restoring normal hepatic insulin metabolism. In addition, among patients on peritoneal dialysis, glucose contained in peritoneal dialysate tends to increase the need for diabetes therapy. Changes in dietary intake and exercise (ie, reduced intake due to anorexia prior to starting dialysis) can also affect the response to administered insulin. Furthermore, the uremic environment can affect methods used to assess glycemic control, and the metabolism of most oral diabetes agents is prolonged, making them more difficult to use.
This topic reviews glycemic targets, methods of monitoring glycemic control, and suggested treatment regimens for patients on hemodialysis and peritoneal dialysis. The treatment of diabetes in kidney transplant recipients is discussed elsewhere (see "Kidney transplantation in adults: Chronic kidney disease (CKD) is associated with insulin resistance and, in advanced CKD, decreased insulin degradation. The latter can lead to a marked decrease in insulin requirement or even the cessation of insulin therapy in patients with type 2 diabetes. Both of these abnormalities are at least partially reversed with the institution of dialysis. (See "Carbohydrate and insulin metabolism in chronic kidney disease".)
MONITORING GLYCEMIC CONTROL
Glycated hemoglobin (A1C) — We monitor glycemic control in patients with diabetes and predialysis chronic kidney disease (CKD) or end-stage renal disease (ESRD) as we do in patients with diabetes and normal kidney function. Thus, we use serial measurements (two to four times yearly) of glycated hemoglobin (hemoglobin A1C, A1C) to assess chronic glycemic control in diabetic patients with predialysis CKD or ESRD
QUESTION :-How to prevent ?
ANSWER :-
* To prevent DM and CKD is to modify lifestyle habits
* Exersise regularly
* Avoid oily and junk foods
* Have adequate water and be hydrated
* monitor sugar levels regularly if Diabetic
*
An early diagnosis
An early diagnosis of diabetes can help your doctor treat the condition before it does more damage to your body. Type 1 diabetes (also known as juvenile or insulin dependent diabetes) is easily diagnosed in its early stages, before kidney damage occurs. However, Type 2 diabetes (also known as adult-onset or non-insulin dependent diabetes) often goes undiagnosed for years. Many people who have Type 2 diabetes do not realize it.
Because Type 2 diabetes may have been present for many years before it is diagnosed, this means the high glucose(sugar) content in the blood has had time to damage the tiny blood vessels in the kidneys. When these blood vessels are damaged, protein that is meant to remain in the body can leak into the urine. This is a condition called microalbuminuria, and it is an early symptom of kidney disease.
If you have been diagnosed with Type 1 or Type 2 diabetes, you should have a microalbumin test done annually. This will help your doctor detect any kidney damage. If your urine tests positive for albumin (a protein), steps can be taken to help prevent more damage to your kidneys.
Control your blood glucose levels
Because the high glucose content in your bloodstream can damage the kidneys, controlling the level of glucose is an important step in keeping the kidneys healthy. This means following the plan your doctor recommends for treating your diabetes. For Type 1 diabetics, getting regular insulin is crucial in keeping glucose levels in check. For Type 2 diabetics, diet and exercise may be the primary treatments for lowering blood sugar levels.
Your doctor may have you test your glucose levels throughout the day. You may be referred to a dietitian, who can help you make healthier food choices. Lowering your intake of sugar is important, especially if you are insulin resistant. Your doctor may also want you to lose excess weight. Follow your doctor’s instructions regarding medicines and testing your glucose levels. If the levels are still too high, tell your doctor so adjustments can be made to your treatment program.
Control your blood pressure levels
If you are diabetic and have been diagnosed with high blood pressure (also known as hypertension), your kidneys have a greater chance of becoming damaged. Patients with high blood pressure and diabetes are more likely to develop nephropathy. This is because high blood pressure places added strain on the tiny blood vessels of the kidneys. Your doctor may prescribe a medicine called an ACE inhibitor to bring down your blood pressure.
Even in diabetic patients who do not have high blood pressure, studies have shown that ACE inhibitors are an effective treatment for kidney disease. Even though you may not have high blood pressure, your doctor may prescribe this medicine for you in order to prevent further strain to your kidneys. If you have any questions or concerns about any medicine that has been prescribed to you, talk with your doctor. Do not stop taking any medicine prescribed to you without talking to your doctor first.
Keep healthy habits
If you have been diagnosed with diabetes, your doctor may ask that you stop certain activities that could worsen your diabetes or lead to high blood pressure. Activities such as smoking and drinking alcohol should be avoided.
Exercise is an excellent habit. Your doctor may recommend exercise as part of your treatment. But before you start a program, ask your doctor if the activity may be right for you.
QUESTION :-What is the cause?
ANSWER:-cause of CKD in DM patients include
- improper maintenance of blood glucose levels
- no proper monitoring
- improper diet qnd exercise
- lack of observation and adequate management
High blood glucose, also called blood sugar, can damage the blood vessels in your kidneys. When the blood vessels are damaged, they don't work as well. Many people with diabetes also develop high blood pressure, which can also damage your kidneys.
- Age and sex can be a risk factor
- intake of alcohol
-heriditory
- lack of health education and knowledge
QUESTION :-What is the pathophysiology?
ANSWER :-due to causes and risk factors
A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased 50%.
The plasma creatinine value will approximately double with a 50% reduction in GFR. For example, a rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL in a patient, although still within the adult reference range, actually represents a loss of 50% of functioning nephron mass.
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 glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with chronic kidney disease (CKD).
Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following:
Systemic hypertension
Nephrotoxins (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], intravenous contrast media)
Decreased perfusion (eg, from severe dehydration or episodes of shock)
Proteinuria (in addition to being a marker of CKD)
Hyperlipidemia
Hyperphosphatemia with calcium phosphate deposition
Smoking
Uncontrolled diabetes
Thaker et al found a strong association between episodes of acute kidney injury (AKI) and cumulative risk for the development of advanced CKD in patients with diabetes mellitus who experienced AKI in multiple hospitalizations. [6] Any AKI versus no AKI was a risk factor for stage 4 CKD, and each additional AKI episode doubled that risk. [6]
Findings from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD. [7] This study used data from 1787 cases of CKD that developed between 1987 and 2004.