Nephrotube Ckd Module End Exam

Iron deficiency is the most common cause of resistant anemia in CKD patients. Chronic kidney disease (CKD) can lead to decreased production and release of erythropoietin, a hormone responsible for stimulating red blood cell production. This can result in anemia. Iron deficiency further exacerbates the anemia as iron is necessary for the production of hemoglobin, the protein in red blood cells that carries oxygen. Therefore, addressing iron deficiency is crucial in managing anemia in CKD patients.

Treatment of anemia can prevent the development of left ventricular hypertrophy. Left ventricular hypertrophy is a condition where the muscle wall of the left ventricle of the heart becomes thickened, which can lead to heart failure. Anemia is a condition characterized by a decrease in red blood cells or hemoglobin levels, which can result in decreased oxygen delivery to tissues, including the heart. By treating anemia and increasing the hemoglobin levels, the oxygen-carrying capacity of the blood is improved, reducing the risk of left ventricular hypertrophy.

The correct answer is to treat the patient with an angiotensin-converting enzyme (ACE) inhibitor to achieve a target blood pressure (BP) of 130/85 mmHg. This recommendation is based on the information provided in the case, which suggests that the patient has hypertension. ACE inhibitors are commonly used to treat hypertension and have been shown to be effective in reducing BP and preventing cardiovascular complications. The target BP of 130/85 mmHg is in line with current guidelines for the management of hypertension.

According to the current National Kidney Foundation Chronic Kidney Disease classification, Stage 2 is characterized by mild reduction in kidney function (GFR 60-89 ml/min/1.73m2) with evidence of kidney damage, such as persistent proteinuria. Since the patient has a stable estimated GFR of 70 ml/min/1.73m2 and persistent trace protein in the urine, he falls into Stage 2 of CKD.

The patient's history of microscopic hematuria and abnormal renal ultrasound findings indicate the presence of chronic kidney disease (CKD). CKD is defined by the presence of kidney damage or decreased kidney function for three months or longer. The presence of blood in the urine (hematuria) and the presence of multiple cysts in both kidneys on ultrasound are consistent with kidney damage. The normal serum creatinine and protein excretion do not exclude the diagnosis of CKD, as early stages of CKD can be asymptomatic and may not cause significant changes in these parameters.

The patient has polycystic kidney disease (PKD) which can lead to decreased production of active vitamin D (calcitriol) by the kidneys. The low serum calcium level and high intact parathyroid hormone (PTH) level indicate secondary hyperparathyroidism, which is commonly seen in CKD. Treatment with calcitriol helps to increase serum calcium levels and suppress PTH secretion, thereby managing secondary hyperparathyroidism. Restricting dietary phosphorus, avoiding calcium-containing phosphate binders, and starting long-term therapy with aluminum hydroxide are not appropriate for this patient. Sevelamer therapy is actually associated with a decreased risk of osteomalacia and bone fractures.

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The correct answer is that serum iron, transferrin saturation, and ferritin should be measured to assess iron stores. In this case, the patient has anemia with a low hemoglobin level and hematocrit, which suggests a deficiency in iron. To confirm this, it is necessary to measure serum iron, transferrin saturation, and ferritin levels. These tests will provide information about the body's iron stores and help guide appropriate treatment for the anemia. The other options are not relevant to the assessment of anemia in this patient with IgA nephropathy.

Acidosis increases calcium loss from bone. In metabolic acidosis, there is decreased pH in the blood, which leads to increased bone resorption and calcium release from the bones. This is due to the body's compensatory mechanism to maintain pH balance by releasing calcium ions from the bones. This can contribute to the development of osteoporosis and increased risk of fractures.

A higher prevalence of traditional risk factors such as hypertension and dyslipidemia account for the increased risk of cardiovascular disease in patients with CKD. This means that patients with CKD are more likely to have conditions like high blood pressure and high cholesterol, which are known risk factors for cardiovascular disease. As a result, they are at a higher risk of developing cardiovascular disease compared to the general population. Additionally, the statement suggests that cardiovascular disease may be a leading cause of death in patients with CKD before they progress to end-stage renal disease.

The answer states that the low GFR in the 78-year-old man is a consequence of aging and he should not be classified as having chronic kidney disease (CKD). This is because as individuals age, there is a natural decline in kidney function, resulting in a lower GFR. In this case, the patient's GFR is 69 ml/min per 1.73 m2, which falls within the range for stage 2 CKD. However, it is important to note that the patient's urinary protein excretion rate is normal, indicating that there is no evidence of kidney damage. Therefore, the low GFR is attributed to aging rather than a pathological condition.

The severity of tubulointerstitial disease is a good predictor of kidney disease progression. This means that the extent of damage and inflammation in the tubules and interstitium of the kidney can help determine the likelihood of the disease progressing. In this case, the patient had severe tubulointerstitial disease on a previous kidney biopsy, suggesting a higher risk of kidney failure in the future. This information is important for managing the patient's condition and making decisions about treatment options.

The patient has biopsy-proven IgA nephropathy and is already experiencing symptoms of fatigue. His kidney function, as indicated by his serum creatinine and GFR, is significantly impaired. Given his young age and the availability of a blood-group compatible sister as a potential kidney donor, a preemptive living donor transplant would be the most appropriate recommendation. This would provide the patient with the best chance of long-term renal function and improved quality of life, compared to starting dialysis or delaying the need for dialysis with a low-protein diet.

In chronic kidney disease (CKD), there is a decrease in the glomerular filtration rate (GFR), which leads to alterations in bone and mineral metabolism. The correct answer states that elevated serum phosphorus inhibits the 1-alpha hydroxylase enzyme in the kidney, which is responsible for the synthesis of calcitriol (active form of vitamin D). This inhibition of calcitriol synthesis can lead to abnormal mineral metabolism. This answer is supported by the understanding that CKD can cause abnormalities in phosphate metabolism, leading to elevated serum phosphorus levels, which in turn can inhibit the production of calcitriol.

The extent of tubulointerstitial disease on biopsy is the best predictor of the patient's risk of progressing to end-stage renal disease (ESRD). Tubulointerstitial disease refers to damage and inflammation in the tubules and interstitial tissue of the kidneys, which can contribute to the progression of kidney disease. The presence and severity of tubulointerstitial disease on biopsy can help determine the extent of kidney damage and the likelihood of progression to ESRD.

The patient in this case has type 2 diabetes and is at increased risk for cardiovascular complications due to his family history and smoking habit. His blood pressure is within the normal range, but his albumin/creatinine ratio is elevated, indicating early kidney damage. Starting treatment with an angiotensin II receptor blocker (ARB) is recommended in this case as ARBs have been shown to slow the progression of kidney disease in patients with diabetes. This treatment choice aims to protect the patient's kidneys and reduce the risk of further complications.

Lowering the target blood pressure (BP) can slow the progression of kidney disease in this patient. The patient has chronic kidney disease (CKD) with a calculated glomerular filtration rate (GFR) of 32 ml/min per 1.73 m2. Lowering the BP can help protect the kidneys by reducing the pressure on the blood vessels in the kidneys, thereby slowing the progression of kidney disease. This is especially important in patients with diabetes and hypertension, as they are at a higher risk for kidney disease progression. Therefore, lowering the target BP is the most correct choice for this patient.

Based on the laboratory test results, the patient has a low hemoglobin level (10.1 g/dl), indicating anemia. The serum iron level (92 mg/dl), transferrin saturation (23%), and ferritin level (130 ng/ml) suggest iron deficiency anemia. The appropriate next step would be to start recombinant erythropoietin therapy, which stimulates red blood cell production, along with oral iron supplementation to address the iron deficiency. This treatment approach aims to increase the patient's hemoglobin level and improve their anemia.

The random spot urine protein/creatinine ratio is misleading because of the low creatinine production. This is because the patient's serum creatinine level is normal, indicating that her kidney function is not impaired. However, the spot urine protein/creatinine ratio is high, suggesting significant proteinuria. This discrepancy can be explained by the low creatinine production, which leads to an artificially elevated protein/creatinine ratio. Therefore, the patient does not have nephrotic range proteinuria.

The correct answer is that intravenous contrast is not contraindicated in patients with CKD. This is because the patient's acute renal failure, indicated by the rise in serum creatinine after receiving IV contrast, is likely due to acute tubular necrosis caused by sepsis and hypotension, rather than contrast-induced nephropathy. The patient's baseline CKD, as indicated by the proteinuria and slightly decreased estimated GFR, is unrelated to the acute renal failure. Therefore, the administration of IV contrast in this case is not contraindicated.