|
| A) | 15% | ||
| B) | 22% | ||
| C) | 44% | ||
| D) | 65% |
Diabetes is the leading cause of kidney failure in the United States, accounting for 44% of new cases [2]. In 2018, 131,636 individuals in the United States began treatment for end-stage renal disease requiring dialysis or transplantation [3]. In the United States, annual end-stage renal disease costs are estimated to be $49.2 billion, with a greater incidence and associated cost among racial minorities [3].
| A) | 2% to 6% | ||
| B) | 15% to 20% | ||
| C) | 25% to 30% | ||
| D) | 40% to 50% |
According to the American Diabetes Association (ADA), as of 2020, 10.5% of the U.S. population, or 34.2 million Americans, have a diagnosis of diabetes. In addition, an estimated 7.3 million people have diabetes but remain undiagnosed [7]. By 2025, it is predicted that 15% to 20% of all Americans will have a diagnosis of diabetes or impaired glucose tolerance [8].
| A) | An HbA1c level of 6.5% | ||
| B) | Two fasting blood glucose levels of 130 mg/dL | ||
| C) | A two-hour glucose challenge result of 140 mg/dL | ||
| D) | A random blood glucose of 210 mg/dL with symptoms of hyperglycemia |
DIAGNOSTIC CRITERIA FOR TYPE 2 DIABETES
| Stage | Fasting Plasma Glucose Level | Two-Hour Postprandial Plasma Glucose Level | Glycated Hemoglobin (HbA1c) |
|---|---|---|---|
| Euglycemia | ≤100 mg/dL | <140 mg/dL | <5.7% |
| Prediabetes | >100 mg/dL but <126 mg/dL | ≥140 mg/dL but <200 mg/dL | 5.7% to 6.4% |
| Diabetesa | ≥126 mg/dL | ≥200 mg/dL | ≥6.5% |
| aA random blood glucose level ≥200 mg/dL with symptoms of hyperglycemia is also indicative of diabetes. | |||
| A) | 70 kDa. | ||
| B) | 90 kDa. | ||
| C) | 0.001 mL. | ||
| D) | 0.000004 mL. |
It is approximated that the glomerular filtration rate (GFR) in a healthy individual with two properly functioning kidneys is 90–120 mL/min/1.73 m2 [20]. The approximate mass cutoff of substances for filtration is 70 kDa [21]. Substances greater than the 70 kDa cutoff are often retained during filtration; smaller particles are excreted in the urine.
| A) | Macula densa | ||
| B) | Loop of Henle | ||
| C) | Bowmen capsule | ||
| D) | Proximal convoluted tubule |
Typically, approximately 30 mL/min of isotonic filtration is delivered to the loop of Henle, where a countercurrent multiplier mechanism achieves concentration of the urine [21]. The loop of Henle is the portion of the nephron formed by the descending and ascending limbs of the renal tubule [20]. This loop passes down into the medulla of the kidney, where secretion of sodium, chloride, and urea takes place. The thick ascending limb is impermeable to water but allows resorption of sodium, chloride, potassium, calcium, and bicarbonate. Due to the low water and high solute resorption in the loop of Henle, the filtration leaves the ascending limb hypo-osmotic [23].
| A) | immune system. | ||
| B) | musculoskeletal system. | ||
| C) | urinary system. | ||
| D) | angiotensin-aldosterone system. |
The kidneys maintain the circulating blood volume by fluid balancing and by altering peripheral vascular resistance via the angiotensin-aldosterone system [23]. First, the sodium concentration in the proximal tubular fluid is sensed at the macula densa, part of the juxtaglomerular apparatus. The juxtaglomerular apparatus also assesses the perfusion pressure, an important indicator of intravascular volume status under normal circumstances. Through the action of these two sensors, either low sodium or low perfusion pressure acts as a stimulus to renin release [21]. Renin, a protease made in the juxtaglomerular cells, cleaves angiotensinogen in the blood to generate angiotensin I, which is then cleaved to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II raises blood pressure by triggering vasoconstriction directly and by stimulating aldosterone secretion, resulting in sodium and water retention by the collecting duct [20]. All of these effects expand the extracellular fluid and consequently renal perfusion pressure, completing a homeostatic negative feedback loop that alleviates the initial stimulus for renin release [21].
| A) | renin release. | ||
| B) | sodium release. | ||
| C) | nitric oxide retention. | ||
| D) | bradykinin inhibition. |
There are other clinically important adaptations to injury. Poor renal perfusion from any cause results in responses that improve perfusion through afferent arteriolar vasodilation and efferent arteriolar vasoconstriction in response to hormonal and neural cues [21]. These regulatory effects are reinforced by inputs sensing sodium balance. Alteration of sodium balance is another way to influence blood pressure and renal perfusion pressure [22]. Sympathetic innervation by the renal nerves influences renin release. Renal prostaglandins play an important role in vasodilation, particularly in individuals with chronically poor renal perfusion [21].
| A) | hypotension. | ||
| B) | poor glycemic control. | ||
| C) | impaired renal blood flow. | ||
| D) | age and history of alcohol abuse. |
Acute renal failure is a heterogeneous group of disorders characterized by widespread, rapid deterioration of renal function, resulting in accumulation of nitrogenous wastes in the blood that customarily would be excreted in the urine [21]. The most common origin of acute renal failure is impaired renal blood flow. In these patients, the GFR decreases in response to lower filtration pressures. Diminished perfusion can result from renal vasoconstriction, hypotension, hypovolemia, hemorrhage, or inadequate cardiac output [24].
| A) | Prerenal | ||
| B) | Perirenal | ||
| C) | Postrenal | ||
| D) | Intrarenal |
There are three etiologic categories of acute renal failure: prerenal, intrarenal, and postrenal.
| A) | Uremia | ||
| B) | Diabetes | ||
| C) | Renal frost | ||
| D) | Sympathetic syndrome |
The clinical manifestations of chronic renal failure are often described using the term uremia. Uremia refers to a number of symptoms caused as a result of declining renal function and the accumulation of toxins in the plasma [24]. It has a number of effects on metabolism, including a decrease in a basal body temperature (perhaps due to decreased sodium, potassium, and ATP activity) and diminished lipoprotein lipase activity with accelerated atherosclerosis [21].
| A) | water. | ||
| B) | sodium. | ||
| C) | potassium. | ||
| D) | phosphorus. |
Excretory failure also results in fluid shifts, with increased intracellular sodium and water and decreased intracellular potassium. These alterations may contribute to subtle alterations in the function of a host of enzymes and transport systems [21].
| A) | Albuminuria | ||
| B) | Hypotension | ||
| C) | Glucotoxicity | ||
| D) | Hyperinsulinemia |
Albuminuria is a well-known marker of poor renal outcomes in individuals with type 2 diabetes [31]. Persistent albuminuria is present in the earliest stage of nephropathy in type 1 diabetes and is a marker for development of nephropathy in type 2 diabetes [21]. Albuminuria has been shown to be a predictor of poor cardiovascular outcomes; therefore, serum albumin should be measured in all individuals with diabetes and hypertension and steps should be taken to suppress albuminuria to prevent further renal and cardiovascular events [31].
| A) | Hypotension | ||
| B) | Glucotoxicity | ||
| C) | Hyperglycemia | ||
| D) | Kimmelstiel Wilson nodules |
Kimmelstiel Wilson nodules (nodular glomerulosclerosis) are a classic feature of diabetic damage to the kidney [32]. If Kimmelstiel Wilson nodes are present on biopsy, this is positive for diabetic nephropathy. The pathology of these nodes is related to histologic renal changes [5]. Progressive histologic changes in glomeruli are indistinguishable in type 1 and type 2 diabetes and occur to some degree in the majority of individuals [33]. The mesangium surrounding the glomerular vessels is increased due to the deposition of basement membrane-like material and can encroach on the glomerular vessels; the afferent and efferent glomerular arteries are also sclerosed. Glomerulosclerosis is usually diffuse; however, in some cases, it is associated with nodular sclerosis [33].
| A) | equilibrium. | ||
| B) | hypoglycemia. | ||
| C) | hyperfiltration. | ||
| D) | changes in mentation. |
Research has demonstrated that hypertension, hyperglycemia, and high triglyceride concentrations are associated with an elevation in albumin-to-creatinine level independent of the type of diabetes [34]. Glucagon and growth hormone are both elevated in poorly controlled diabetes and have been shown to produce glomerular hyperfiltration, a phase that generally precedes glomerular alterations in patients with type 1 diabetes. Changes in circulating levels of angiotensin II, catecholamines, and prostaglandins, or altered responsiveness to these vasoactive hormones, may also result in hyperfiltration [1]. It is unclear whether this early hyperfiltration phase occurs in type 2 diabetes. It has been proposed that the presence of atherosclerotic lesions in older individuals with type 2 diabetes may prevent hyperfiltration and thus account for the lower incidence of overt clinical nephropathy in these individuals [35,36,37].
| A) | 10–20 mg urinary protein per day. | ||
| B) | 100–200 mg urinary protein per day. | ||
| C) | 300–500 mg urinary protein per day. | ||
| D) | 4–6 mg urinary protein per day. |
If glomerular lesions worsen, proteinuria increases and overt nephropathy develops. Diabetic nephropathy is defined clinically by the presence of more than 300–500 mg of urinary protein per day, an amount that can be detected by routine urinalysis [1]. In diabetic nephropathy, proteinuria continues to increase as renal function decreases. Therefore, end-stage renal disease is preceded by massive, nephritic-range proteinuria (greater than 4 mg/dL) [1]. Renal hemodynamic changes play a role in the pathogenesis of diabetic kidney disease.
| A) | 120/70 mm Hg. | ||
| B) | 130/70 mm Hg. | ||
| C) | 140/80 mm Hg. | ||
| D) | 160/90 mm Hg. |
Blood pressure management is also an important part of preventing renal disease in patients with diabetes. A target blood pressure of less than 130/80 mm Hg has been advised. However, tighter control is necessary in the presence of nephropathy; 120/70 mm Hg is suggested for these patients [1].
| A) | Androgenic | ||
| B) | Antidiuretic | ||
| C) | Erythropoietin | ||
| D) | Adrenocortical |
Anemia may occur in individuals with diabetic nephropathy even prior to the onset of advanced renal failure. This tendency is the result of erythropoietin deficiency [54]. Erythropoietin, typically manufactured in the kidney, is a hormone that stimulates the bone marrow to produce red blood cells [1]. Erythropoiesis-stimulating agent treatment should be initiated when hemoglobin levels are less than 11 g/dL, with a target hemoglobin level of 11–12 g/dL and a target hematocrit of 30% to 33% [56]. The potential risk of hypertension with erythropoietin therapy should be taken into consideration prior to initiating treatment [54,57]. Monthly hematocrit measurements are necessary during therapy so the dosage can be titrated as necessary. Measurements of serum iron and ferritin levels are recommended before initiating erythropoietin therapy and periodically during treatment to determine whether iron therapy should be initiated.
| A) | Inability to anticoagulate | ||
| B) | Hemodynamic instability | ||
| C) | Relapse or drug resistance | ||
| D) | Lack of access to circulation |
Hemodialysis is contraindicated if any of the following are present [23]:
Hemodynamic instability
Inability to anticoagulate
Lack of access to circulation
| A) | A living relative | ||
| B) | A living unrelated donor | ||
| C) | A tissue-matched primate | ||
| D) | A suitable cadaveric donor |
Kidney transplant can be performed using a kidney from a living relative donor, a living unrelated donor, or a suitable cadaveric donor [1]. Allocation of all transplants in the United States is managed by the United Network for Organ Sharing (UNOS). Kidney transplant guidelines place the highest considerations on histocompatibility and time spent on the transplant list [76]. The median adult wait time for a cadaver kidney is just over four years [3]. When the kidney is procured from the donor or cadaver, the ureter, renal vein, and renal artery are dissected, leaving as much length as possible [23].
| A) | at diagnosis. | ||
| B) | within 1 year of diagnosis. | ||
| C) | within 5 years of diagnosis. | ||
| D) | within 10 years of diagnosis. |
An intensive and multifactorial management approach is required for patients with diabetes and renal disease in order to address all risk determinants. This strategy should include lifestyle modifications (e.g., smoking cessation, weight management and reduction, increased physical activity, dietary changes) coupled with therapeutic achievement of evidence-based blood pressure, blood glucose, and lipid goals [77]. All individuals with type 1 or type 2 diabetes must be educated regarding the need for screening to assess kidney function regularly. In patients with type 1 diabetes, screening should be completed within five years of diagnosis and then annually thereafter. For patients with type 2 diabetes, screening should begin at diagnosis and continue annually thereafter [1].