Benign prostatic hyperplasia (BPH) is defined as enlargement of the prostate as a result of the excessive proliferation of its stromal and glandular cells.
This condition is extremely common in elderly men. Clinically, BPH gives rise to lower urinary tract symptoms (LUTS) including hesitancy, urgency, and incomplete voiding, due to compression of the prostatic urethra.
Lines of management include watchful waiting, pharmacotherapy, and prostatic resection. If left untreated, acute urinary retention (AUR), hematuria, renal calculi, and acute or chronic renal failure may ensue.
Acute Kidney Injury (AKI) is marked by an abrupt, severe decline of kidney function (in less than 48 hours). This condition manifests as a sudden rise in serum creatinine levels, reduced or absent urine output, and the need for dialysis.
The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines 2012 define AKI as any of the following: an increase in serum creatinine (SCr) by at least 0.3 mg/dL (26.5 micromol/L) within 48 hours; OR an increase in SCr of 1.5-fold over the baseline known or presumed to have occurred within the preceding seven days; OR A urine volume of 0.5 mL/kg/h or less for a period of six hours.
The etiopathology is divided into three major groups: pre-renal causes due to decreased renal perfusion (most often caused by depleted volume), renal causes due to pathological processes within the kidneys, and post-renal causes due to obstruction or retention of urine distal to the kidney.
By mechanism, the etiological classification is as follows: ischemia-re
perfusion injury, sepsis, or nephrotoxicity.
Elimination of the underlying cause is the mainstay of treatment. Dialysis or renal replacement therapy may be indicated for many of these patients.
The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines stage AKI based on either the serum creatinine or urine output, as follows:
Stage 1: A rise in the serum creatinine to 1.5-1.9 times the baseline OR a rise in serum creatinine of at least 0.3 mg/dL (26.5 micromoles/L), OR a urine output of 0.5 mL/kg/h or less for 6-12 hours
Stage 2: A rise in serum creatinine to 2.0-2.9 times the baseline OR a urine output of 0.5 mL/kg/h or less for at least 12 hours
Stage 3: A rise in serum creatinine to 3.0 times the baseline OR a rise in serum creatinine to at least 4.0 mg/dL (353.6 micromoles/L) OR the initiation of renal replacement therapy OR, in patients younger than 18 years, a decrease in the eGFR to 35 mL/min or less per 1.73 m2
The basic pathophysiology of AKI is a rapid decline in kidney function, Thus, a baseline serum creatinine (bSCr) is required to reflect the patient's kidney's function prior to the onset of the condition, to confirm the diagnosis, and to determine the stage of the disease. However, this value is often unavailable and may need to be calculated.
One such method of calculation, known as back-estimation, utilizes the Modification of Diet in Renal Disease (MDRD) formula and presumes that there is no available information regarding prior kidney function and/or pre-existing renal disease. Other methods utilize the first SCr measured at the time of hospital admission and the nadir SCr during the first three days of ICU stay.
The term chronic kidney disease (CKD) defines kidney damage that persists for three months or more. An excess of albumin in the urine (albuminuria) and subnormal kidney function manifested by a reduced glomerular filtration rate (GFR) are the usual presentations.
Both acute kidney injury (AKI) and CKD are known to lead to end-stage renal disease (ESRD) and, ultimately, the need for dialysis or renal replacement therapy.
AKI was once thought to be a risk factor for CKD; however, recent studies have found that the two are not mutually causative. Yet, they do share similar risk factors, such as metabolic syndrome, obesity, hypertension, diabetes, and cardiovascular disease. A patient recovering from AKI may later suffer from CKD despite normal kidney function.
Acute uric acid nephropathy, a subtype of AKI, is frequently observed in patients suffering from malignancies and/or undergoing chemotherapy, as a complication of tumor lysis syndrome. Rarely, it may occur as a complication of rhabdomyolysis or post cardiac surgery in children.
Urate crystallization leads to AKI primarily by intrarenal obstruction and local inflammation; this process usually occurs at serum uric acid levels of 12 mg/dL and above.
Treatments include lowering the uric acid levels with recombinant uricase, xanthine oxidase inhibitors, and/or dialysis. Alkalinization of the urine is also beneficial, as it increases the solubility of urate.
Cassava contains linamarin, a cyanogenic compound that can sometimes be metabolized into hydrogen cyanide.
Patients will commonly present with upper motor neuron abnormalities.
Djenkolism is a form of acute kidney injury that occurs from the excessive ingestion of djenkol beans (Archidendron pauciflorum), also known as jering beans or dogfruit.
The bean has a strong odor and is considered a delicacy in many southeast Asian countries. It contains djenkolic acid that crystallizes in the kidney, ureter, or urethra, especially in an acidic environment.
Susceptibility to this condition varies from one individual to another. Risk factors remain largely unknown, except for gender (males are seven times as likely to suffer from djenkolism than females). The pathophysiology remains uncertain as well; most patients do not have crystals in their urine samples and so the disease is thought to also have an autoimmune cause.
Symptoms vary and include colicky abdominal pain, hematuria, dysuria, flatulence, vomiting, diarrhea or constipation. A urinalysis will usually demonstrate albumin, epithelial cells, casts, erythrocytes, and, occasionally, needle-shaped crystals.
The rationale behind using bicarbonate for djenkolism is to increase the urinary pH since djenkolic acid is known to crystallize in an acidic environment. However, its use has not been supported by substantial evidence to date.
Research documenting the benefits of furosemide for AKI is limited, and Kidney Disease: Improving Global Outcomes (KDIGO) does not recommend the use of diuretics for patients with AKI with no evidence of volume overload.
Fluid resuscitation is widely used for patients with AKI. However, the risk of fluid overload remains a concern. The aim is to restore the systemic BP and, in turn, the adequacy of kidney perfusion.
Signs of volume overload vary depending on the onset and severity of the disease. Acute fluid overload presents with rapid-onset pulmonary edema with audible rales, while chronic fluid overload presents with fatigue, dyspnea, and slow-onset pulmonary edema with pitting peripheral (pedal) edema.