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Kidney Structure

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The kidneys are two large bean-shaped organs located in the upper abdomen. They filter the blood several times a day to remove toxins and rebalance water and electrolytes of the circulatory system via the renal veins. The kidneys receive blood directly from the heart via the renal arteries. These arteries enter the kidney at the hilum, the concave surface of the bean, where they branch and divide into smaller vessels and capillaries.
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External Anatomy of the Kidney01:21

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The kidneys are a pair of bean-shaped organs in the human body that play a critical role in maintaining overall health. They filter out waste products from the blood, regulate blood pressure, maintain electrolyte balance, and stimulate the production of red blood cells.
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Internal Anatomy of the Kidney01:12

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The kidneys are essential organs in the human body, performing a myriad of tasks that maintain homeostasis and overall health.
Anatomical Position and Dimensions
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A kidney transplant is a surgical approach that involves replacing a non-functioning kidney with a healthy one from a donor. This procedure is often a treatment option for end-stage renal disease (ESRD) patients. The method requires careful recipient selection, including evaluating various medical and psychosocial factors. These criteria vary between transplant centers but generally include assessments of the patient's overall health, adherence to medical recommendations, and lifestyle...
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Anatomy of the Genitourinary System I: Kidneys and Ureters01:11

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The upper urinary system comprises two kidneys and two ureters, which are crucial in filtering blood and forming urine.KidneysLocation and Structure:The kidneys are two bean-shaped organs positioned behind the peritoneum on either side of the spine.Kidneys are between the 12th thoracic (T12) and the 3rd lumbar (L3) vertebrae.The position of the liver causes the right kidney to sit slightly lower than the left.Protective Layers:Each kidney is enveloped in a tough, fibrous membrane called the...
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Acute Kidney Injury I: Introduction01:22

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Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
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Hypoparathyroidism and the Kidney.

Munro Peacock1

  • 1Department of Medicine, Division of Endocrinology, Indiana University School of Medicine, 1120 West Michigan Street Cl 365, Indianapolis, IN 46202, USA.

Endocrinology and Metabolism Clinics of North America
|November 5, 2018
PubMed
Summary
This summary is machine-generated.

Hypoparathyroidism causes low calcium and high phosphate due to lack of parathyroid hormone (PTH) action. PTH treatment may offer fewer side effects than vitamin D-thiazide therapy.

Keywords:
1,25 dihydroxy vitamin DCalcium homeostasisHypoparathyroidismKidneyPTHPhosphate homeostasisTubular reabsorption calciumTubular reabsorption phosphate

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Area of Science:

  • Biochemistry
  • Endocrinology
  • Nephrology

Background:

  • Hypoparathyroidism is characterized by hypocalcemia and hyperphosphatemia.
  • These biochemical changes result from the absence of parathyroid hormone (PTH) action on renal calcium and phosphate transport.
  • PTH secretion is regulated by circulating calcium levels, not phosphate levels.

Purpose of the Study:

  • To elucidate the biochemical consequences of absent parathyroid hormone (PTH) action.
  • To describe the clinical manifestations of hypocalcemia.
  • To discuss the risks associated with current treatments and explore potential alternatives.

Main Methods:

  • Review of biochemical mechanisms in hypoparathyroidism.
  • Analysis of the effects of parathyroid hormone (PTH) on renal calcium and phosphate handling.
  • Evaluation of clinical outcomes associated with vitamin D-thiazide therapy versus PTH treatment.

Main Results:

  • Lack of PTH action leads to dysregulated renal calcium and phosphate reabsorption, causing hypocalcemia and hyperphosphatemia.
  • Hypocalcemia manifests as neuromuscular disturbances, including epilepsy, tetany, and paresthesia.
  • Hyperphosphatemia, while often subclinical, contributes to ectopic mineralization and renal damage, particularly with vitamin D-thiazide treatment.

Conclusions:

  • The biochemical hallmark of hypoparathyroidism is the direct result of impaired parathyroid hormone (PTH) activity in the kidneys.
  • Current treatments like vitamin D and thiazides carry risks of ectopic mineralization and renal damage.
  • Parathyroid hormone (PTH) replacement therapy presents a potential alternative with a favorable side effect profile.