Diabetic nephropathy (DN) is a well-described complication of diabetes mellitus and the leading cause of end stage renal disease (ESRD). Although increased albuminuria has been the gold standard for screening, data suggests that renal damage starts long before the onset of clinically apparent increases in macro and even micro-albuminuria. Clinical practice guidelines for the prevention of DN have been traditionally focused on the control of serum glucose, blood pressure and dyslipidemia, with some focus on the renin-angiotensin-aldosterone system (RAAS) as a main target for successful therapy. Recent evidence has led to a better understanding of the underlying mechanisms of the pathophysiology of this disease and suggests that various novels pathways can be targeted to delay and even prevent the progression of DN. Hence a more comprehensive therapeutic approach to therapy is on the horizon, carrying the promise for a more successful and impactful management. This review will highlight new insights into the pathophysiology, clinical aspects and future diagnostic and therapeutic modalities for DN.

Purpose of reviewTo give an update on the latest developments regarding rare adverse effects of bisphosphonate therapy. Recent findingsRecent studies covering osteonecrosis of the jaw (ONJ) and atypical femoral fractures (AFFs) provided several updates to the literature. Identification of ONJ in large population databases is a challenge but based on one systematic review, the ICD-10 diagnosis code K10.2 (inflammatory conditions of the jaw) seems to be the most commonly used code for this condition. Duration of bisphosphonate therapy was determined to be an important predictor of AFFs. Appropriate duration of therapy followed by a timely drug holiday was shown to be the best strategy for improving bone mineral density and reducing fracture risk, while minimizing risk of rare adverse effects of therapy. The utility of bone turnover markers as a monitoring tool during drug holidays needs to be further investigated. SummaryONJ and AFFs are two of the rare adverse effects associated with bisphosphonate therapy. Population-level trends of bisphosphonate use suggest a decline in prescriptions, pointing to broad fears of these side effects. Careful patient evaluation, duration of bisphosphonate therapy, and use of drug holidays can help limit any risk associated with therapy.

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Background: Transient osteoporosis is an uncommon and self-limited clinical syndrome characterized by acute joint pain with evidence of bone marrow edema on MRI. It predominantly affects healthy middle-aged men or women in the third trimester of pregnancy. The hips, knee, foot and ankle are affected in decreasing order of frequency. Pathophysiology is unknown but multiple etiologies such as ischemia, neurogenic compression or impaired venous return have been proposed. Classically, it is unilateral and bilateral in only 20%-40% of cases. It has been reported to periodically involve different joints over time with one report showing the progression to regional migratory osteoporosis in at least 20% of patients. There are no specific biomarkers to aid with diagnosis, MRI shows diffuse bone marrow edema sometimes associated with joint effusion with infrequent subchondral microfractures. Other etiologies to consider for bone marrow edema include osteomyelitis, avascular necrosis, trauma, tumors and inflammatory arthropathy. Transient osteoporosis can be self- limiting however, bisphosphonate use has been associated with shortened recovery time. In our patient given lack of access to his previous records to review and ascertain his previous diagnosis, his diagnosis of record was transient osteoporosis rather than regional migratory osteoporosis. Clinical Case: A 47 yo male presented to clinic with complaint of left ankle pain. Pain initially noted when he tripped and fell one year ago. Initial x-rays did not reveal any fractures. He was unable to weight bear due to pain although he had full range of motion at the ankle with a normal neurological and vascular exam of the foot. Due to persistence of pain, an MRI was done which showed cutaneous edema around the medial and lateral aspects of the ankle, trace tibiotalar joint effusion, marrow edema in the distal tibia and navicular with no acute fracture or definite evidence of avascular necrosis. On further questioning he reported a previous history of hip pain at age 32 and 41 with no preceding trauma. X-rays were negative for fracture and MRI showed marrow edema. Symptoms resolved after a few weeks with possible treatment with Alendronate. With the current presentation biochemical work up including Vitamin D, PTH, 24-hour urine calcium, electrolytes, phosphorus and alkaline phosphatase was unremarkable. Given the marrow edema reported on MRI, absence of fracture, osteochondral lesion or recent trauma transient osteoporosis was diagnosed. Given the duration of symptoms he was treated with Reclast 5mg IV once and reported 80% improvement in ankle pain during follow up 4 weeks later. Conclusion: It is important to identify transient osteoporosis and regional migratory osteoporosis to prevent unnecessary medical or surgical therapy.